International Cytokinecytokinesociety.org/wp-content/uploads/2016/11/ICIS-2013-Final-Program.pdf · International Cytokine and Interferon Society Confirmed Invited Speakers James

Inaugural Meeting of the

International Cytokineand

Interferon Society (ICIS)Formerly the International Cytokine Society (ICS) and

International Society for Interferon and Cytokine Research (ISICR)

September 29 – October 3, 2013San Francisco, California, USA

See Cytokine, Vol. 63, Iss. 3, 2013 for abstracts 1-297; S1 – S7.

See Cytokine, Vol. 63, Iss. 3, 2013 for abstracts 1-297; S1 – S7.

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08-0023-08.indd 1 9/3/13 10:31 AM

Inaugural Meeting of theInternational Cytokine

andInterferon Society (ICIS)

Formerly the International Cytokine Society (ICS) and International Society for Interferon and Cytokine Research (ISICR)

September 29 – October 3, 2013San Francisco, California, USA

Scientific Organizing CommitteeWarren Leonard, Bethesda, Maryland, USA

Sarah Gaffen, Pittsburgh, Pennsylvania, USA Karen Mossman, Hamilton, Ontario, CanadaRobert Schreiber, St. Louis, Missouri, USA

Scientific Advisory CommitteeDaniel J. Cua, Palo Alto, California, USA

Charles A. Dinarello, Denver, Colorado, USA Vishva M. Dixit, South San Francisco, California, USA

Charles Egwuagu, Bethesda, Maryland, USA Douglas J. Hilton, Melbourne, Australia

David E. Levy, New York, New York, USA Luke O’Neill, Dublin, Ireland

Ellen V. Rothenberg, Pasadena, California, USA Federica Sallusto, Bellinzona, Switzerland

Charles Samuel, Santa Barbara, California, USA Tadatsugu Taniguchi, Tokyo, Japan

Howard A. Young, Bethesda, Maryland, USA

Awards CommitteeMarion Kasaian, Cambridge, Massachusetts, USA

Jennifer Towne, Seattle, Washington, USARobert Silverman, Cleveland, Ohio, USA

Keynote SpeakerK. Christopher Garcia, Stanford, California, USA

Sherwood M. Reichard, Secretariat

BioMedical PressP.O. Box 3271

Augusta, Georgia 30914

International Cytokine and Interferon Society

Confirmed Invited SpeakersJames Allison, MD Anderson Cancer Center, TX USA

David Artis, University of Pennsylvania, Philadelphia, PA USA

Jody Baron, University of California, San Francisco, CA USA

Greg Barton, University of California, Berkeley, CA USA

Yasmine Belkaid, National Institutes of Health, Bethesda, MD USA

Jeff Bluestone, University of California, San Francisco, CA USA

Andrew Bowie, Trinity College, Dublin, Ireland

Marco Colonna, Washington University, St. Louis, MO USA

Carolyn Coyne, University of Pittsburgh, Pittsburgh, PA USA

Shane Crotty, La Jolla Institute Allergy & Immunology, La Jolla, CA USA

Jason Cyster, University of California, San Francisco, CA USA

Vishva Dixit, Genentech, South San Francisco, CA USA

Charles Egwuagu, National Institutes of Health, Bethesda, MD USA

Katherine Fitzgerald, University of Massachusetts, Worcester, MA USA

Richard Flavell, Yale University, New Haven, CT USA

Thomas Gajewski, University of Chicago, Chicago, IL USA

Michael Gale, University of Washington, Seattle, WA USA

K. Christopher Garcia, Stanford University, Stanford, CA USA

Sankar Ghosh, Columbia University, New York, NY USA

Thomas Hamilton, Cleveland Clinic, Cleveland, OH USA

Lothar Hennighausen, National Institutes of Health, Bethesda, MD USA

Chris Hunter, University of Pennsylvania, Philadelphia, PA USA

Akiko Iwasaki, Yale University, New Haven, CT USA

Brendan Jenkins, Monash University, Victoria, Australia

Susan Kaech, Yale University, New Haven, CT USA

Tadamitsu Kishimoto, Osaka University, Osaka, Japan

Lewis Lanier, University of California, San Francisco, CA USA

Warren Leonard, National Institutes of Health, Bethesda, MD USA

Xiaoxia Li, Cleveland Clinic, Cleveland, OH USA

Eddy F.Y. Liew, University of Glasgow, Glasgow, Scotland

Xin Lin, MD Anderson Cancer Center, Houston, TX USA

Daniel Littman, New York University, New York, NY USA

Richard Locksley, University of California, San Francisco, CA USA

Angel Lopez, Center for Cancer Biology, Adelaide, Australia

Averil Ma, University of California, San Francisco, CA USA

Tak Mak, University of Toronto, Toronto, Canada

Grant McFadden, University of Florida, Gainesville, FL USA

Karen Mossman, McMaster University, Hamilton, Canada

Anne O’Garra, National Institute for Medical Research, London, United Kingdom

John O’Shea, National Institutes of Health, Bethesda, MD USA

Michael B.A. Oldstone, Scripps Institute, La Jolla, CA, USA

Wenjun Ouyang, Genentech, South San Francisco, CA USA

Søren R. Paludan, Aarhus University, Aarhus, Denmark

Fiona Powrie, University of Oxford, Oxford, United Kingdom

Freddy Radtke, ISREC, Lausanne, Switzerland

Federica Sallusto, Institute for Research in Biomedicine, Bellinzona, Switzerland

Robert Schreiber, Washington University, St. Louis, MO, USA

Alan Sher, National Institutes of Health, Bethesda, MD USA

Stephen Smale, University of California, Los Angeles, CA USA

George Stark, Cleveland Clinic Foundation, Cleveland, OH USA

Tadatsugu Taniguchi, University of Tokyo, Tokyo, Japan

Thomas Tedder, Duke University, Durham, NC USA

Kevin Tracey, Feinstein Institute, Manhasset, NY USA

Giorgio Trinchieri, National Cancer Institute, Frederick, MD USA

Emil Unanue, Washington University, St. Louis, MO USA

Thomas Waldmann, National Institutes of Health, Bethesda, MD USA

David Wallach, Weizmann Institute, Rehovot, Israel

Amy Weinmann, University of Washington, Seattle, WA USA

Hua Yu, Beckman Research Institute, City of Hope, Duarte, CA USA

Albert Zlotnik, University of California, Irvine, CA USA


Program at a GlanceSunday, September 29th9:30-4:00 pm ICIS Council and Committee Meetings (Seacliff A; Seacliff B)12:00 pm Registration Opens 5:30 – 8:15 pm Opening Session (Grand A) •ICISAwards •HonoraryMembershipAwards •2013MilsteinAwards •KeynoteLecture8:15 – 9:45 pm Welcome Reception (Grand Foyer)

Monday, September 30th 8:30 – 10:30 am Plenary Session I (Grand A) •Cytokines&Microbes–CommensalstoPathogens10:30 -11:00 am Coffee Break – visit the exhibitors (Pacific Concourse)11:00 – 1:00 pm Concurrent Symposia •SymposiumT1:InflammatoryCytokinesandtheInflammasome(GrandA) • SymposiumT2:ImmuneInvasion(GrandB/C)1:00–2:00pm LunchBreak(onown)1:00–2:00pm WorkshopforTrainees:PanelDiscussiononCareerOptions inScience-LimitedNumberofBoxLunches(Seacliff)2:00 – 3:30 pm Concurrent Minisymposia (Selected from Submitted Abstracts)2:00–3:30pm •Minisymposium1(GrandA) •Minisymposium2(GrandB/C)3:30 – 4:00 pm Coffee Break – visit the exhibitors (Pacific Concourse) 4:00 – 6:15 pm International Cytokine and Interferon Society (ICIS) Inaugural Special Scientific Symposium (Grand A)6:30 – 8:00 pm Poster Session I (Pacific Concourse) with wine and cheese

Tuesday, October 1st8:30 –10:30 am Plenary Session 2 (Grand A) •Cytokines–BasicMechanisms10:30 – 11:00 am Coffee Break – visit the exhibitors (Pacific Concourse)11:00 – 1:00 pm Concurrent Symposia •SymposiumT3:TCellSubsets(GrandA) • SymposiumT4:Interferons(GrandB/C)1:00–2:00pm LunchBreak(onown)


1:00–2:00pm JICREditorialBoardLuncheon(Seacliff)2:00 – 3:30 pm Concurrent Minisymposia (Selected from Submitted Abstracts) •Minisymposium3(GrandA) •Minisymposium4(GrandB/C)3:30 – 4:00 pm Coffee Break – visit the exhibitors (Pacific Concourse)4:00 – 6:00 pm Concurrent Symposia •SymposiumT5–Autoimmunity(GrandA) •SymposiumT6–ChemokinesandtheirReceptors(GrandB/C)6:00 – 7:30 pm Poster Session II (Pacific Concourse) with wine and cheese7:30–9:00pm SpecialNetworkingReceptionforStudents,Postdocsand New(1stYear)Faculty–TicketsRequired(SeacliffA&B)

WEDNESDAY, OCTOBER 2nd

8:30 –10:30 am Plenary Session III (Grand A) •CytokineFundamentals–Signaling,Expression and Epigenetics (Grand A)10:30 -11:00am Coffee Break – visit the exhibitors (Pacific Concourse)11:00 -1:00 pm Concurrent Symposia • SymposiumT7–CytokinesinInfections(GrandA) •SymposiumT8–CytokineandInterferonGene RegulationandSignalingI(GrandB/C)1:00–2:00pm LunchBreak(onown)2:00 – 3:45 pm Concurrent Minisymposia •Minisymposium5(GrandA) •Minisymposium6(GrandB/C)3:45 – 4:15 pm Coffee Break – visit the exhibitors (Pacific Concourse)4:15 – 5:45 pm Concurrent Symposia •SymposiumT9-PatternRecognition(GrandA) •SymposiumT10–CytokineandInterferonGeneRegulation andSignalingII(GrandB/C) 6:00 – 7:30 pm Poster Session III (Pacific Concourse) with wine and cheese 8:00–12:00M BanquetandEntertainment(GrandB/C)

Thursday, October 3rd8:30-11:30am • FromBenchtoBedside11:30 am Closing Remarks


SPONSORS AND EXHIBITORS CYTOKINES 2013

Abbott PharmaceuticalAbcam *

AbFrontier*Adipogen International/Chimerigen*

Amgen USABioBasic, Inc.*

Biogen IdecBioLegend *

Bio-Rad Laboratories*Boehringer-IngelheimBristol Myer Squibb

CSO Tempero PharmaceuticalsCytoSorbents Corporation*

eBioscience, An Affymetrix Company*Elsevier BV*

EMD Millipore*EMD Serono (Merck)

Ensemble TherapeuticsGenentech (Roche)

JICR (Mary Ann Liebert, Inc.)*Lilly USA, LLC.

Medimmune (Astra Zeneca)Miltenyi Biotec, Inc.*

National Institutes of HealthNature Reviews ImmunologyNovoprotein Scientific,Inc.*

PBL InterferonSource *PeproTech, Inc.*

PfizerPlexBio (Genemed)*R&D Systems, Inc.*

Sanguine BioSciences*Science Signaling

Singulex*Sino Biological, Inc.*

*ExhibitorInternational Cytokine and Interferon Society

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EXHIBITORSAbcam Booth #6Aris Krikelis, CFA Marketing Coordinator Representative:330 Cambridge Science Park John ConstableCambridge, CB4 OFLUnited KingdomTel: +44 1223 646000Fax: +44 1223 215215Website: www.Abcam.com

Abcam is a provider of protein research tools and services, with an unrivalled range of products and expert technical support, enabling scientists to analyze living cells at the molecular level and improving the understanding of health and disease. Abcam is committed to providing scientists with an extensive choice of reagents and tools, with the most comprehensive, honest and up-to-date datasheets and customer reviews, fast delivery and helpful customer service & technical support. The company’s catalog of products includes primary and secondary antibodies, proteins, peptides, lysates, biochemicals, immunoassays and other kits.

AbFrontier Booth #25Sean Lee Representative:11F, Byucksan Digital Valley 5th Sean LeeGason-Dong 60-73 Geum Cheon-Gu,Seoul, South KoreaTel: 82-2-2140-3366Fax:82-2-2140-3330Website: abfrontier.com

AbFrontier is a brand name of Young In Frontier Co., Ltd., South Korea’s leading supplier of catalog and custom antibodies and high quality ELISA kits. AbFrontier’s specialty is custom antibody manufacturing and custom development of cutting–edge products (including ELISA kits) in its own research center. AbFrontier is a manufacturer of cutting-edge ROS signaling and Cytokine research reagents.

Adipogen International/Chimerigen Booth #7 Jim Rodgers, Operations Manager Representative:11588 Sorrento Valley Road, Suite 16 Georges ChappuisSan Diego, CA 92121, USATel: 858-457-8383Fax; 858-457-8484Website: www.adipogen.com

Manufacturer of new and innovative life science reagents in the areas of cytokines, cancer immunology inflammation, metabolic syndrome (diabetes, obesity) and stem cell biology.A major focus is on innovative and advanced ELISA kits and new antibiody technologies (recombinant antibodies). Our partner company. Chimerigen, is a leading manufacturer of cytokines and Fc proteins with long half life in vivo.


BioLegend Booth #2-3Sharon Sasaki, Marketing Representatives:Communications Manager Avi Perna9727 Pacific Heights Blvd Hortensia SotoSan Diego, CA 92121 USA Shaoquan JiTel: 858-768-5810 Miguel TamFax: 877-455-9587 Gene Lay Website: www.Biolegend.com

BioLegend provides world-class antibodies, proteins, assays, and custom research solutions. Request bulk quotes for Bioactive Recombinant Cytokines and Chemokines and new Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibodies for in vivo assays. New ELISA Kits and Sets include TGF-β family (total, free active, latent, LAP), IP-10 and other chemokines, mouse IFN-β. Obtain superior performance on the violet laser with our complete family of Brilliant Violet™ antibody conjugates. We offer new LEGENDScreen™ Human and Mouse Cell Screening (PE) Kits, new Zombie Aqua™ and Zombie Yellow™ Fixable Viability Kits, and personalized multicolor flow cytometry panel design.

Bio-Rad Laboratories Booth #14Olga Padilla, Event & Tradeshow Manager Representative:2000 Alfred Nobel Drive Brett HouserHercules, CA 94547Tel: 510-741-5052Fax: 510-741-5630Website: www.bio-rad.com

Since the 1950s, Bio-Rad has been a leader in life science research, developing assays emphasizing quality, reliability, productivity, and ease of use. Bio-Rad’s Bio-Plex multiplex system (built on Luminex xMAP technology) uses magnetic bead-based immunoassays to measure up to 100 analytes in a single sample. The Bio-Plex system allows researchers to obtain results with less time and effort, using lower sample volumes in a high-throughput format. The Bio-Plex assays are available for cytokines, chemokines, growth factors, cell signaling, hormones, ligands and receptors, and disease biomarkers for cancer,autoimmune disorders, metabolic and kidney toxicity.


Bio Basic, Inc. Booth #10Jennifer Wang, Manager Representative:20 Konrad Cres Senthil SaravanamuthuMarkham, Ontario, L3R 8T4CanadaTel: 905-474-4493Fax: 905-474-5794Website: www.biobasic.comUS Headquarters: 4160 Bailey AvenueAmherst, NY 14226 USA

Bio Basic Inc. was founded in 1990 as a biochemical manufacturer in Toronto, Canada. Since 1995, Bio Basic Inc. has grown into a manufacturer of various life science research products including recombinant proteins such as cytokines and growth factors. Bio Basic Inc now serves as a one-stop-shop for our life science customers by offering wide range of high quality products and services at lowest prices. To date, Bio Basic Inc. including its subsidiaries has over 900 employees, seven laboratories, three factory buildings, 40 international distributors and over 10,000 customers worldwide. Bio Basic Inc’s US headquarters is located in Amherst, NY. Bio Basic has manufacturing plants in Canada, USA and Asia. Bio Basic Product categories: Biochemicals, Molecular Biology Kits, PCR Related Products, DNA & RNA Modifying Enzymes, DNA, RNA & Protein Markers & Cloning Vectors, Pre-cast gels, Recombinant Proteins (cytokines & growth factors), Protein Related Products, Microbiological Culture medium, Labwares Bio Basic Services: Oligo synthesis, Gene synthesis, Sub-cloning, Mutagenesis, Peptide synthesis, Standard DNA, sequencing, Protein purification, Custom antibody generation (poly & monoclonal)

CytoSorbents Corporation Booth #20 Humayra Ali, Senior Manager, Business Representative: Development & Scientific Affairs Humayra Ali7 Deer Park Drive, Suite K Monmouth Junction, NJ 08852 USATel: 732-895-4024Fax: 732-329-8650Website: www.cytosorbents.com

CytoSorbents Corporation (Ticker Symbol OTC BB: CTSO) is a U.S.-based, publicly-traded business, that has developed a very biocompatible, highly porous polymer bead technology used to purify cytokines and other toxins from blood, bodily fluids and other liquid medium. Our flagship product is CytoSorb®, a hemoadsorption cartridge designed to treat critical care illnesses where systemic cytokines and inflammatory mediators are elevated such as sepsis, acute respiratory distress syndrome (ARDS), acute lung injury (ALI), severe influenza, burn injury, trauma, severe acute pancreatitis and other life-threatening inflammatory conditions. CytoSorb® is currently approved and being commercialized in the European Union.


eBioscience, An Affymetrix Company Booth #8 Laurie Durlester, Manager, Event Management Representatives:10255 Science Center Drive Stacey BordersSan Diego, CA 92121, USA Matt SlaterTel: 888-899-1371 Matt SchifanoFax: 858-642-2046 Peggy JustWebsite: www.ebioscience.com Markus MiholitseBioscience, an Affymetrix Company, develops and manufactures over 13,000high-quality antibodies, recombinant proteins, immunoassays and multiplex assays at ISO certified facilities worldwide for research and clinical use that accelerate scientific discovery in the areas of immunology and oncology.

Elsevier BV Booth #5Jolanda de Rijk, Exhibitions Coordinator Representative:Radarweg 29 Jenny HenzenAmsterdam, 1043NX NetherlandsTel: +31 20 485 3798Fax: +31 20 485 3228Website: Elsevier.com

Cytokine is published by Elsevier, a world-leading provider of scientific, technical and medical information products and services. It is an official Journal of the International Cytokine and Interferon Society (ICIS). Devoted exclusively to the study of the molecular biology, biochemistry, immunology, diagnostic and clinical applications of all known interleukins, hematopoietic factors, growth factors, cytotoxins, interferons and new cytokines, Cytokine provides comprehensive coverage of cytokines and their receptors, 12 times a year by publishing original high quality refereed scientific papers from prominent investigators in both the academic and industrial sectors.

EMD Millipore Booth #22-23Jeffrey Owen, Manager, NA Representatives: Trade Show and Sales Support Mike Vaughn 290 Concord Road Thad BakerBilerica, MA 01821 USA Debra MaclvorTel: 800-854-3417 Wen-Rong LieFax: 800-645-5439 Jun MaWebsite: www.emdmillipore.com

EMD Millipore is the Life Science division of Merck KGaA of Germany, supporting research, development and production of biotech and pharmaceutical drug therapies. We support customers with antibodies, ELISAs and multiplex detection assays for cytokine/chemokine quantification. We also offer cell-based activity assays and cellular analysis platforms for measuring cytokine signaling.


Mary Ann Liebert, Inc. Booth #21Lisa Pierce Representative:140 Huguenot Street Vicki CohnNew Rochelle, NY 10801Tel: 914-740-2100 Fax: 914-740-2105Website: www.liebertpub.com

Journal of Interferon & Cytokine Research, an Official journal of the International Cytokine and Interferon Society (ICIS), provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs and the identification and function of IFN-Inducible genes.

Miltenyi Biotec, Inc. Booth #19Marketing Communications Coordinator Representatives:6125 Cornerstone Court East Kent JordanSan Diego, CA 92121 USA, Alusha MamchakTel:852-202-0758 Irena GeurseWebsite: www.miltenyibiotec.com Emad MalikMiltenyi Biotec’s mission is to improve scientific understanding and medical progress. We provide products and services that advance biomedical research and cellular therapy. Honoring this mission drives our commitment to support the translation of basic research into therapy in the areas of immunology, cancer, neuroscience and stem cell biology. We innovate products that address sample preparation, separation of cells and their analysis, and that advance the concept of cellular therapy. “Researchers working for researchers” is our promise to provide pioneering products to our customers.

Novoprotein Scientific, Inc. Booth #4Yufang Shao, Vice-President Representative:47 Maple Street, Suite L-8 Yufang ShaoSummit, NJ 07901, USA Tel: 973-671-8010Fax: 888-253-6691Website: www.novoprotein.com

Novoprotein Scientific, Inc. is a protein-centric biotech company which offers a comprehensive portfolio of custom protein services and carries a catalog of 700 plus cytokine/recombinant proteins. The service scope includes protein expression, process development, custom antibody production, protein modification and protein crystallization. The capacity of the four well-established protein expression systems: E.coli, yeast, baculovirus/insect cell and mammalian cell systems has reached gram scale. Novoprotein has built its successful track record with an impressive 80% success rate over 1100 projects. The company has retained large pharma partners and biotech companies over years. Novoprotein products cover a broad range of biological aspects from immunology, stem cell, oncology and neurobiology. Novoprotein has an overall 95% customer satisfaction rate for its quality, service and cost. Recently GEN news reported the opening of Novoprotein US office in Summit, NJ for US marketing. The US office has further improved smooth communication between the customers and the company and increased the direct exposure of the great service and products the company can offer to the life sciences.


PBL InterferonSource Booth #18Hong-Gee Lee Representatives:Senior Product Manager & Technical Support Scientist Thomas LavoiePBL InterferonSource Stephen Parent131 Ethel Road Robert Pestka Piscataway, NJ 08854 USA Tel: 732-777-9123 ext. 129 Fax:732- 777-9141 Website: www.interferonsource.com

PBL InterferonSource, your trusted source for interferon ELISAs, proteins, antibodies, and assay services, is becoming PBL Assay Science! As PBL’s product lines expand to include additional cytokine targets, new technologies, and expanded assay services, our scope is broadening. We invite you to visit with our scientists (Booth 18) at the ICIS exhibition to see how we can address your challenging assay problems.

PeproTech, Inc. Booth #1Heather Giordano, Marketing Coordinator Representative:5 Crescent Avenue Genevieve Soares Rocky Hill, NJ 08553Tel: 800-436-9910Fax: 609-497-0321Website: www.peprotech.com

PeproTech manufactures an extensive line of Recombinant Human, Murine and Rat Proteins, Animal-Free Recombinant Proteins, Monoclonal Antibodies, Affinity Purified Polyclonal Antibodies, Affinity Purified Biotinylated Polyclonal Antibodies, ELISA Development Kits, Cytokine Packages, Stem Cell Kits and Cell Culture Media Products.

PlexBio Booth #11Peter Luu, Head USA Branch Representative:458 Carlton Court Peter LuuSouth San Francisco, CA 94080, USATel: 650-952-0110Fax: 650-952-1060Website: www.plexbio.com

PlexBio Co., Ltd is a biotechnology company with Asia headquarters in Taipei, Taiwan and US headquarters in South San Francisco. It was established in 2010 to provide powerful, innovative bioassay solutions for the life science and diagnostic industries by leveraging cutting-edge multiplex technologies for both research and IVD use. The PlexBio DigiPlex™is a robust optical imaging system that is both highly effective and easy to use. The complex machine is simple to maintain – no wash or waste fluid management is required – and it accurately decodes beads through high-contrast imaging. The system is compatible with any protein- or nucleic acid-based assays using PlexBio’s multiplex barcoded magnetic beads. The DigiPlex™ comes pre-installed with the DeXipher™ software, which includes instrument control and calibration, quick read function, and data export for 128-plex beads. By combining paramagnetic barcoded polymer beads with our optical imaging system and software, it becomes possible to obtain sensitive, specific results for multiple analytes quickly and with low sample volumes. The IntelliPlex™ technology saves precious time, labor, reagents, and sample for applications in both life science and in vitro diagnostics.


R&D Systems,Inc, Booth #12-13Tracey Husted,Trade Show Coordinator Representatives:614 McKinley Place, NE Karen RootMinneapolis, MN 55413 USA David SehyTel: 612-379-2956 Gerry AndrosFax: 612-379-6580Website: www.RnDsystems.com

R&D Systems is a leading supplier of cell biology research reagents. We offer a wide array of products including recombinant and natural proteins, antibiodies, ELISAs, cell culture reagents, and kits for cell selection, apoptosis/cell viability assays, and multianalyte profiling.

Sanguine Biosciences Booth #15Jake Loewenheim, VP of Sales Representative: 28903 North Avenue Paine Jake LoewenheimValencia, CA 91355, USA David Wintern BeimerTel: 650-868-1512Website: www.sanguinebio.com

Sanguine Biosciences is a company focused on sourcing biospecimen focused on patients with autoimmune/inflammatory diseases. We provide inventory banked disease and custom collection services for fresh and frozen whole blood, PBMCs serum, plasma, RNA/DNA, and Leukopak related samples.

Singulex, Inc. Booth # 24Natasha Ritz, Marketing Coordinator Representative1701 Harbor Bay Parkway, Suite 200 Joel AliphonAlameda, CA 94502 USATel: 510-995-4612Website: www.singulex.com

Singulex, Inc., is a leader in advanced biomarker research, deploying high-definition digital immunoassay technology enhancing the clinical utility of biomarkers by accurately, precisely and reliably quantifying previously undetectable biomarkers with LLoQ down to the sub-picogram levels – even in healthy population. The flexible Singulex Solution includes the Erenna Immunoassay System, High-Definition Immunoassays, and a full range of Custom Services to accelerate your biomarker research from discovery to clinical trials.

Sino Biological Inc. Booth # 9Jack Lu, Brand Manager Representative:14 Zhong He Street BDA Charles Xiaoxiang Zhu Beijing, 100176 China Amy Hong QueTel: +86-10-51029968-838Fax: +86-10-51029969Website: www.sinobiological.com

Sino Biological, Inc, is one of the largest cDNA, recombinant protein and antibody product manufacturers and suppliers to biomedical and pharmaceutical research in the world. It has now commercialized more than 10,000 peoducts, including 3000 recombinant protein and 3000 antibody products, and offering a comprehensive set of value-added and cost-effective premium quality solutions (CRO services and reagents) to accelerate life science research and biological product development worldwide.


P R O G R A M 2013 Inaugural Meeting of the International Cytokine and Interferon Society

(ICIS)formed by the merger of the International Cytokine Society and the

International Society of Interferon and Cytokine Research

From Molecular Mechanisms to Human DiseaseSan Francisco, California, USA

September 29 – October 3, 2013

Organizers:Warren J. Leonard, National Heart, Lung and Blood Institute, NIH

Sarah L. Gaffen, University of PittsburghKaren L. Mossman, McMaster University

Robert D. Schreiber, Washington University in St. Louis

Sunday, September 29, 20139:30 – 4:30 pm ICIS Council and Committee Meetings Seacliff A Seacliff B

12.00 – 8:30 pm REGISTRATION Grand Ballroom Foyer

5:30 – 8:15 pm OPENING SESSION Grand Ballroom A

5:30 – 5:40 pm Opening Remarks and Welcome Warren Leonard for the Organizing Committee

5:40 – 6:00 pm Opening Ceremony: ICIS AWARDS Charles Samuel and Luke O’Neill Co-Presidents, ICIS

6:00 - 6:30 pm ICIS HONORARY MEMBERSHIP AWARDS

Dynamiting Viruses with Mx Otto Haller University of Freiburg, Freiburg, Germany Warren Leonard NationalHeart,LungandBloodInstitute,NIH,Bethesda,MD,USA (TalktobegivenMondayafternoonintheICISInaugural Special Scientific Symposium)

6:30 -7:15 pm 2013 MILSTEIN AWARDS

Fine Tuning Interferon Signaling -Lessons Learned from Other Systems Paul Hertzog Monash Institute of Medical Research, Clayton, Victoria, Australia Mechanisms of interferon signaling Leon Platanias NorthwesternUniversitySchoolofMedicine,Chicago,IL,USA


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Sunday, September 29, continued

Xiaoxia Li ClevelandClinicFoundation,Cleveland,OH,USA (TalktobegivenWednesdayafternooninSymposiumT10: Cytokine and Interferon Gene Regulation and Signaling II)

Keynote Lecture Sponsored by R&D Systems

7:15 – 8:15 pm KEYNOTE LECTURE: Interrogating and Manipulating Cytokine Receptor Signaling with Structure and Protein Engineering: IFN and IL-2 K. Christopher Garcia, HHMIandStanfordUniversity,PaloAlto,CA,USA Introducedby:WarrenLeonard,NHLBI,NIH,Bethesda,MD,USA

8:15 – 9:45 pm WELCOME RECEPTION Grand Ballroom B/C

Monday, September 30, 2013

8:00 am– 7:00 pm Registration Grand Ballroom Foyer

8:30 – 10:30 am PLENARY SESSION I: Cytokines & Microbes - Grand Ballroom A Commensals to Pathogens Chairs: Anne O’Garra,NIMR,MRC,London,UnitedKingdomand Paul Hertzog, Monash Institute of Medical Research, Clayton, Victoria, Australia

8:30 - 9:00 am Regulation of Barrier Immunity, Paper S-8 DavidArtis,UniversityofPennsylvania,PA,USA

9:00 – 9:30 am Inflammasomes in Dysbiosis, Health and Disease, Paper S-29 RichardFlavell,HHMIandYaleUniversity,NewHaven,CT,USA

9:30 – 10:00 am The Immune Response in Tuberculosis; Lessons Learned from Mouse Models and Human Disease Anne O’Garra

10:00 – 10:30 am Induction of Th17 Cells by Commensal Microbes DanLittman,HHMIandNewYorkUniversity,NewYork,NY,USA

10:30 – 11:00 am Coffee Break – visit with the exhibitors Pacific Concourse

11:00am – 1:00 pm CONCURRENT SYMPOSIA

SYMPOSIUM T1: Inflammatory Cytokines and the Inflammasome Grand Ballroom A Chairs: Katherine Fitzgerald, University of Massachusetts,Worcester, MA, USA and Vishva Dixit, Genentech, South San Francisco, CA, USA

11:00 – 11:30 am Long Non-Coding RNA: a New Layer of Complexity in Gene Regulation in the Innate Immune System KateFitzgerald 11:30am–12:00N Reflex Control of Inflammasome Activity KevinTracey,FeinsteinInstitute,NewYork,NY,USA

12:00 – 12:30 pm The Role of Cytokines in Infection and Inflammation, Paper S-9 EddyF.Y.Liew,UniversityofGlasgow,Glasgow,Scotland,UnitedKingdom


12:30 – 1:00 pm Non-Canonical Inflammasome Activation Targets Caspase-11, Paper S-10 VishvaDixit

11:00 am – 1:00 pm CONCURRENT SYMPOSIA

SYMPOSIUM T2: Immune Evasion Grand B/C Chairs: Curt Horvath,NorthwesternUniversity,Evanston,IL,USAand Carolyn Coyne, University of Pittsburgh, PA, USA

11:00 – 11:30 am How Enteroviruses Navigate the Dangerous World of Pattern Recognition Receptor Signaling Carolyn Coyne

11:30am–12:00N Lindenmann Looked for a Herring and Found a Smallmouth Bass. We Looked for Dr. Jekyll and Found Mr. Hyde: Interferon Induces Persistent Viral Infection, Paper S-7 MichaelB.A.Oldstone,ScrippsResearchInstitute,LaJolla,CA,USA

12:00 – 12:30 pm Control of Innate Antiviral Immunity by HIV-1 Michael Gale, University of Washington, Seattle, WA, USA

12:30 – 1:00 pm Cytokine Synergy: An Underappreciated Player in Innate Anti-Viral Immunity GrantMcFadden,UniversityofFlorida,Gainesville,FL,USA

1:00–2:00pm LunchBreak(LunchonOwn)

1:00 – 2:00pm Workshop for Trainees: Panel Discussion on Career Options in Science Seacliff (LimitedNumberofBoxLunches) Panel Members: Jenifer Towne (Amgen) Mandy McGeachy (University of Pittsburgh), Vishva Dixit (Genentech), Fang Shen (Janssen), Howard Young (NCI), Olive Leavy (Nature Reviews Immunology)

2:00 - 3:30 pm CONCURRENT MINISYMPOSIA (Selected from Submitted Abstracts)

2:00 - 3:30 pm MINISYMPOSIUM 1 Grand Ballroom A Papers 1, 3, 16, 34, 43, 44 and 78 Chairs: Partha Biswas, University of Pittsburgh, PA, USA and Matthias Ernst,WalterandElizaHallInstituteofMedicalResearch,Parkville,Australia

ED LEONARD AWARD2:00 - 2:15 pm Chemokine Networks Regulate the Balance of Pro-and Anti-Tumor Granulocytes that Determine Metastatic Progression in Breast Cancer Models, Paper 1 SwarnaliAcharyya,MemorialSloan-KetteringCancerCenter,NewYork,NY,USA

2:15 - 2:30 pm Integrin-Linked Kinase Modulates LPS-Induced TNFα Production via Regulation of p65 Phosphorylation at Serine 536 during NF-kB Activation, Paper 3 Afsar Ahmed, Monash Institute of Medical Research, Victoria, Australia

ICIS POSTDOCTORAL INVESTIGATOR AWARD, 3rd Place2:30 – 2:45 pm MIR-17~92 Promotes T Follicular Helper Cell Differentiation and Represses Subset-Inappropriate Gene Expression, Paper 16 DirkBaumjohann,UniversityofCalifornia,SanFrancisco,CA,USA


Monday, September 30, continued

2:45 -3:00 pm LincRNA-Cox2 is a Long Noncoding RNA Induced by TLRs that Mediates Both Activation and Repression of Immune Response Genes, Paper 34 Susan Carpenter, University of Massachusetts Medical School, Worcester, MA, USA

3:00 – 3:15 pm Interferon-Dependent Increase in STAT1, STAT2, and IRF9 Prolongs Resistance to Viruses and DNA Damage, Paper 44 HyeonJooCheon,LernerResearchInstitute,Cleveland,OH,USA

3:15 – 3:30 pm Therapeutic Inhibition of Gp130/Jak/Stat3-Dependent Cytokine Signaling Suppresses WNT-Dependent Colon Cancer Formation, Paper 78 Matthias Ernst

2:00 – 3:45 pm MINISYMPOSIUM 2 Grand B/C Papers 71, 82, 91, 94, 96, 129 and 51 Chairs: Lionel Ivashkiv,WeillCornellMedicalCollege,NewYork,NY,USAand Simon Jones,CardiffUniversity,Cardiff,UK

ICIS YOUNG INVESTIGATOR AWARD2:00 – 2:15 pm Mechanisms of IL-23 Mediated Th17 Inflammation, Paper 71 Mandy McGeachy, University of Pittsburgh, Pittsburgh, PA, USA

2:15 – 2:30 pm IL-36PromotesMyeloidCellInfiltration,ActivationandInflammatoryActivityinSkin, Paper 82 Andrew Johnston, University of Michigan School of Medicine, Ann Arbor, MI, USA

2:30 – 2:45 pm Homotypic T-T Synapses Promote Collective CD8+ T Cell Differentiation through Exchange of IFN gamma, Paper 91 Audrey Gérard, University of California San Francisco, San Francisco, CA, USA

2:45 – 3:00 pm Interleukin-22 Mediates Protection during a Murine Model of Cutaneous Leishmaniasis, Paper 94 Ciara Gimblet, University of Pennsylvania, Philadelphia, PA, USA

3:00 – 3:15 pm Evolutionary Conservation of STING, an Innate Immune Effector and DNA Sensor, in Drosophila Melanogaster, Paper 96 AlanGoodman,UniversityofMiamiSchoolofMedicine,Miami,FL,USA

3:15 – 3:30 pm IFN-g and TNF Alter Epigenetic Landscapes to Control TLR-Induced Transcriptional Responses in Macrophages, Paper 129 LionelIvashkiv

ICIS OUTSTANDING SCHOLAR AWARD, 3rd PLACE3:30 – 3:45 pm Toll-Like Receptor Stimulated Macrophages Intrinsically Control Inflammatory Cytokine Production via Cd39-Based Mechanism, Paper 51 HeatherCohen,UniversityofMaryland,CollegePark,MD,USA

3:45 – 4:15 pm Coffee Break – visit with the exhibitors Pacific Concourse

4:15 – 6:30 pm International Cytokine and Interferon Society (ICIS) Grand Ballroom A Inaugural Special Scientific Symposium Chair: Jan Vilcek,NewYorkUniversitySchoolofMedicine,NewYork,NY,USA

4:15 – 4:25 pm Introduction Jan Vilcek



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I4:25 – 4:55 pm Classical and Non-Classical Cytokines in the Regulation of Innate Immunity, Paper S-11 TadatsuguTaniguchi,UniversityofTokyo,Tokyo,Japan

2013 ICIS HONORARY MEMBERSHIP AWARD4:55 – 5:25 pm The Common γ Chain Family of Cytokines: From Human Disease to Complex Transcriptional Regulation via STAT Proteins WarrenLeonard, NationalHeart,LungandBloodInstitute,NIH,Bethesda,MD,USA

5:25 – 5:55 pm How STAT-Dependent Signals are Prolonged GeorgeStark,ClevelandClinicFoundation,Cleveland,OH,USA

5:55 – 6:25 pm The TNF Family: Novel Signaling Mechanisms Shared with Other Cytokines and Unique Functional Role, Paper S-12 DavidWallach,WeizmannInstitute,Rehovot,Israel

6:25 – 6:30 pm Closing

6:30 – 8:00 pm POSTER SESSION I (with wine and cheese) Pacific Concourse Papers: 1–30, 32-88, 90-113

Chemokine Networks Regulate the Balance of Pro-and Anti-Tumor Granulocytes that Determine Metastatic Progression in Breast Cancer Models, Paper 1Swarnali Acharyya1,PaulinaWojnarowicz1,DanMacalinao1,RayaKhanin2, Zvika Granot4, Robert Benezra1 and Joan Massagué1,3, 1Cancer Biology and Genetics Program, 2Bioinformatics Program Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA, 3Howard Hughes Medical Institute, Chevy Chase, MD 21205, USA, 4The Hebrew University of Jerusalem.

TheP-TEFb-DependentGeneCodingforIL-1βisMoreSensitivetoCellularMetabolismthanthatoftheBRD4-DependentTNFα-CodingGene, Paper 2JurajAdamik1,GillianM.Tannahill2, An-Jey A. Su1,LukeA.O’Neill2,DeborahL.Galson3 and Philip E. Auron1, 1 Department of Biological Sciences, Duquesne University, Pittsburgh, Pennsylvania, USA, 2School of Biochemistry and Immunology, Trinity College Dublin, Dublin, Ireland, 3University of Pittsburgh Cancer Center & School of Medicine, Pittsburgh, Pennsylvania, USA

Integrin-Linked Kinase Modulates LPS-Induced TNFα Production via Regulation of p65 Phosphorylation at Serine 536 during NF-kB Activation, Paper 3Afsar U. Ahmed,GregoryE.HanniganandBryanR.Williams,Centre for Cancer Research, Monash Institute of Medical Research, Clayton, Victoria 3164, Australia

Bacterial Driven Inhibition of IL-12p40 in Primary Human Cells via Modulation of IRF1 and IRF8 Independent of GPCR Signaling and IL-10, Paper 4J. B. Alinger, R. Ireland and C.M. Bosio, Immunity to Pulmonary Pathogens Section, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, MT, USA, 59840

REST Negatively and ISGF3 Positively Regulates the Human STAT1 Gene in Melanoma, Paper 5JamesAmalraj1, Samuel J. Cutler1, Ibtisam Ghazawi1, Glen M. Boyle2 and Stephen J. Ralph1,1School of Medical Science and Genomics Research Centre, Griffith Health Institute, Griffith University, Gold Coast Campus, Queensland, Australia, 2Drug Discovery Group, Queensland Institute of Medical Research, Herston, Queensland, Australia

Innate Immune Responses in Human Dendritic Cells Induced by H9N2 Avian Influenza Virus, Paper 6Veera Arilahti,IlkkaJulkunen,ThediZieglerandPamelaÖsterlund,Virology Unit, National Institute for Health and Welfare (THL), Helsinki, Finland

Cell-Specific Action of Extracellular HMGB1 in Sterile Inflammation of Rat Testis, Paper 7Ferial Aslani1, Andreas Meinhardt1, Sudhanshu Bhushan1,Hans-ChristianSchuppe2,andMonikaFijak1, 1Department of Anatomy and Cell Biology, Justus-Liebig-University, Giessen, Germany, 2Department of Urology, Pediatric Urology and Andrology, Justus-Liebig University of Giessen, Giessen, Germany



Epigenetic Regulation of Th-17 Differentiation, Paper 8Patricia A. Assis,SatoshiUeha,MatthewSchallerandSteveL.Kunkel,University of Michigan Medical School, Department of Pathology, Ann Arbor, MI, USA

MicroRNAs Mediated-Regulation of Mycobacteria-Induced Cytokines Production, Paper 9K.Y.Au1,JamesC.B.Li1, 2 AllanS.Y.Lau1, 2, 1Cytokine Biology Group, Department of Paediatrics and Adolescent Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, People’s Republic of China; 2BioScreening Unit, LKS Faculty of Medicine,The University of Hong Kong, Hong Kong Special Administrative Region, People’s Republic of China

RecombinantAlpha-1Antitrypsin-Fc(AAT-Fc)InhibitsCandida-InducedIL1βSecretionfromHumanCD14Monocytes:Comparison to Plasma-Derived AAT and Caspase 1 Inhibition, Paper 10TaniaAzam1,Jaewoo,Hong2,LeoA.B.Joosten3,SuzhaoLi1,Soo-HyunKim2,andCharles,A.Dinarello1,3, 1Department of Medicine, University of Colorado Denver, Aurora, Colorado USA, 2Institute of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea, 3Department of Internal Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands

Modulation of Immunity against Genital Herpes Simplex Virus, Paper 11MahmoudKarimiAzardaryany1,2, Amanda WS Yeung3,ThomasAsshurst1,2,ShaneRThomas3,andNicholasJCKing1,2, 1 Viral Immunopathology Unit, Discipline of Pathology, School of medical Sciences, The University of Sydney, NSW, Australia, 2 The Bosch Institute, The University of Sydney, NSW, Australia, 3 Centre for Vascular Research, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia

IL-37 Protects Against Obesity-Induced Inflammation and Insulin Resistance, Paper 12DovBBallak1, SuzhaoLi2,JannaAvanDiepen1, Alexander R Moschen3, HenryJansen1,AnnekeHijmans1, Gert-Jan Groenhof1, Philip Bufler4,SanderKersten5,LeoABJoosten1,HerbertTilg3,CharlesADinarello1,2,MihaiGNetea1,CeesJTack1, and Rinke Stienstra1,5, 1Department of Internal Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands. 2Department of Medicine, University of Colorado Denver, Aurora, Colorado, USA. 3Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Innsbruck, Austria. 4Children’s Hospital, Ludwig-Maximilians University, Munich, Germany. 5Department of Human Nutrition, Wageningen University, Wageningen, The Netherlands

Effects of Temperature and pH on IL-1 Stability, Paper 13Adriana Barba-Montoya1,2, Stanislava Panova1,2, Emmanuel Pinteaux2 and Alexander P. Golovanov1,2, 1Manchester Institute of Biotechnology, University of Manchester, Manchester UK, 2Faculty of Life Sciences, University of Manchester, Manchester UK

Inhibition of P53 by Kaposi’s Sarcoma-Associated Herpesvirus-Encoded VIRF3: From Transcriptional Repression to Proteasome-Mediated Degradation, Paper 14Petra Baresova, Jana Musilova, and BarboraLubyova,Charles University, First Faculty of Medicine, Institute of Immunology and Microbiology, Prague, Czech Republic

An Intron of IRF-8 Harbors Myeloid Lineage Specific Regulatory Element that is Regulated by Dynamic Chromatin Architecture, Paper 15OferBarnea-Yizhar,NitsanFourier,AvivaAzriel,SigalRam,andBen-ZionLevi, Department of Biotechnology and Food Engineering, Technion - Israel Institute of Technology, Haifa, Israel

MIR-17~92 Promotes T Follicular Helper Cell Differentiation and Represses Subset-Inappropriate Gene Expression, Paper 16DirkBaumjohann1,RobinKageyama1, Jonathan M. Clingan2,3, Malika M. Morar4, Sana Patel1,DimitrideKouchkovsky4, Oliver Bannard5, Jeffrey A. Bluestone4,6, Mehrdad Matloubian2,KMarkAnsel1,7andLukasT.Jeker4,6,7, 1Department of Microbiology & Immunology, Sandler Asthma Basic Research Center, University of California San Francisco, San Francisco, CA, USA, 2Division of Rheumatology, Department of Medicine, and Rosalind Russell Medical Research Center for Arthritis, University of California, San Francisco, San Francisco, CA, USA, 3Graduate Program in Biomedical Sciences, University of California, San Francisco, CA, USA, 4Diabetes Center and Department of Medicine, University of California San Francisco, San Francisco, CA, USA, 5Department of Microbiology & Immunology, Howard Hughes Medical Institute, University of California, San Francisco, CA, USA, 6Department of Pathology, University of California San Francisco, San Francisco, CA, USA, 7Equal contribution



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IBifunctional Role of Interferon Inducible IFI16 Protein Inside and Outside of Endothelial Cells, Paper 17Mandar Bawadekar1,ValentinaDell’Oste2, Francesca Gugliesi2,DeborahGatti2, MarcoDeAndrea1,2, Valeria Caneparo1,3,SantoLandolfo2 and Marisa Gariglio1,3 , 1Department of Translational Medicine & Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Medical School of Novara-Italy, 2Department of Public Health and Pediatric Sciences, Medical School of Turin- Italy, 3NoToPharm s.r.l. Colleretto Giacosa, Ivrea-Italy

Characterization of Human Interferon-Alpha Subtypes and Mutants, Paper 18Joseph Bekisz1,DanielEichberg1,MichaelDolan2,TongmaoZhao1andKathrynC.Zoon1, 1 Cytokine Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 2Bioinformatics & Computational Bioscience Branch, National Institute of Allergyand Infectious Diseases, National Institutes of Health, Bethesda, MD

B Cell Activation during Behçet Disease: Possible BAFF Involvement in Pathogenesis, Paper 19H.Belguendouz1,D.Messaoudene1,K.Lahmar-Belguendouz1,M.L.Ahmedi1,D.Hartani2, F. Otmani3,O.S.Lahlou-Boukoffa1, Z.Djeraba1, P. Youinou4, C.Touil-Boukoffa1 1’Cytokines & NO Synthases’ team, LBCM, USTHB, Algiers, Algeria, 2Clinique d’ophtalmologie, CHU Mustapha Bacha, Algiers, Algeria, 3Service deMedecine interne, CHU Mustapha bacha, Algiers, Algeria, 4Laboratory of Immunology, Brest University Medical School Hospital, Brest, France

Heterodimeric IL-15 Regulates the Balance of Effector and Regulatory Cells, Favoring Anti-Tumor Responses, Paper 20Cristina Bergamaschi1, Stephanie Chen2, Antonio Valentin1,VirajKulkarni2, Jenifer Bear2, Margherita Rosati1, Candido Alicea2, RachelKellyBeach1,2, Raymond Sowder3, Elena Chertova3,BarbaraK.Felber1,andGeorgeN.Pavlakis2, 1Human Retrovirus Pathogenesis Section and 2Human Retrovirus Section, Vaccine Branch, CCR, NCI; 3Retroviral Protein Chemistry Core, AIDS and Cancer Virus Program, SAIC-Frederick, Inc., FNLCR, Frederick, MD

Interferon-Mediated Potentiation of SMAC Mimetic Compound Cytotoxicity by Oncolytic Virotherapy, Paper 21ShawnT.Beug1,VeraA.Tang1,HermanC.Cheung1,FabriceLeBoeuf2, John C. Bell2,EricC.LaCasse1 and Robert G. Korneluk1, 1Apoptosis Research Centre, Children’s Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada, 2Centre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada

The Role of STAT1 in Macrophages/Neutrophils in the Response to Murine Cytomegalovirus Infection, Paper 22Mario Biaggio1,CarolineLassnig1,2, Ursula Reichart1,2, Rita Rom1,AstridKrmpotic3,StipanJonjic3, Birgit Strobl1 and Mathias Müller1,2, 1Institute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria, 2Biomodels Austria, University of Veterinary Medicine, Vienna, Austria, 3Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Croatia

Complement Component C5a Permits the Co-Existence of Pathogenic Th17 Cells and Type I Interferon in Lupus, Paper 23Partha S. Biswas,SudeshPawaria,KellyMaersandMarcC.Levesque,Department of Medicine, University of Pittsburgh, Pittsburgh, PA USA

STING, not Type I IFN Signaling, is Required for the Mucosal Adjuvant Activity of Cyclic-di-GMP in vivo, Paper 24Steven Blaaubober, Vincent Gabrielle, LeiJin, Center for Immunology and Microbial Disease, Albany Medical College, Albany, NY, USA

STAT2 and IRF9-Dependent IFN-I Signaling Restores ISRE-Mediated Transcription and Anti-Viral Activity Independent of STAT1, Paper 25KatarzynaBłaszczyk1,AdamOlejnik1, Stefan Chmielewski1,KajaKostyrko1, Joanna Wesoly2,Chien-KuoLee3andHansA.R.Bluyssen1, 1Department of Human Molecular Genetics and 2Laboratory of High Throughput Technologies, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland, 3Graduate Institute of Immunology, National Taiwan University College of Medicine, Taipei, Taiwan



Role of the Long Pentraxin PTX3 in Fibrosarcoma Development and Progression, Paper 26E. Bonavita1, S. Gentile1,N.Polentarutti1, F. Feruglio1,F.Pasqualini1,M.Nebuloni3, S, Jaillon1, A. Mantovani1, 2 and C. Garlanda1, 1Laboratory of Immunology and Inflammation, Humanitas Clinical and Research Center, Rozzano, Italy, 20089; 2Department of Translational Medicine, University of Milan, Milan, Italy, 20122. 3L. Sacco Department of Medical Sciences, University of Milan, Milan, Italy, 20122

Altered Immune Modulation is Key to Alcoholic Liver Disease Development and Severity: A Northeast India Based Study, Paper 27Moumita Bose1, RamieHBegum3,TarunBasumatary3,AnjanKumarSaikia1,4,JagatSinghTerron5,ManabDeka1,2, Shyam Sundar Swargiary1, Subhash Medhi2,andSujoyBose1, 1 Department of Biotechnology, Gauhati University, Guwahati, Assam, India,2 Department of Biological Science, IST, Gauhati University, Guwahati, Assam, India,3 Department of Life Science and Bioinformatics, Assam University, Diphu campus, Diphu Assam, India, 4 Medicinal and Gastroenterological unit, Central Hospital, NF Railway, Guwahati, Assam, India, 5 Civil Hospital, Diphu, Assam, India

Mechanisms of Triggering Receptor Expressed on Myeloid Cells-2 (TREM-2) Regulation by Transforming Growth Factor- β1andInterleukin-4;ANewRoleforTREM-2InMatrixMetalloproteinaseRegulation, Paper 28Jenna M. Bradley1,FlorineSquirrell1,DarrenW.Sexton2, Maria A. O’Connell1, 1 School of Pharmacy and 2 Biomedical Research Centre, University of East Anglia, Norwich Research Park, Norwich, UK

Impact of HSV-1 Induced VEGF-A on Corneal Lymphangiogenesis during the Development of Herpetic Stromal Keratitis, Paper 29KatieM.Bryant-Hudson1andDanielJ.J.Carr1,2, 1Department of Ophthalmology, 2Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA

Anti-IL-37 Antibody Abrogates the Protection in IL-37 Transgenic Mice to LPS-Induced Septic Shock, Paper 30Ana-Maria Bulau1, Andrea Gruschka1, Rahel Schwaiger1,CharlesADinarello2 and Philip Bufler1, 1Department of Pediatrics, Dr. von Hauner Children’s Hospital, Ludwig-Maximilians-University, Munich, Germany, 2University of Colorado Denver, Aurora, Colorado, USA

IRF7-Dependent, Type I IFN (IFN-I) Production Induces Lethal Immune-Mediated Disease in STAT1 KO Mice Infected with LCMV, Paper 31IainL.Campbell,WenLiandMarkusJ.Hofer,School of Molecular Bioscience, University of Sydney, NSW, Australia

Chain Specific Polyubiquitination by βTrcp Utlizing Diverse E2 Ubiquitin Conjugating Enzymes Regulatesthe Endocyto-sis of the INFAR1 Chain of Type I Interferon Receptor, Paper 33Christopher J. Carbone,BentleyVarghese,HuiZhengandSergeY.Fuchs, Department of Animal Biology and Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA

LincRNA-Cox2 is a Long Noncoding RNA Induced by TLRs that Mediates Both Activation and Repression of Immune Response Genes, Paper 34Susan Carpenter1,2,ManinjayAtianand1,DanielAiello1, Emiliano Ricci3, Pallavi Gandhi1 ,LisaL.Hall4, Meg Byron4, Brian Monks1,MeabhHenry-Bezy1,LukeA.JO’Neill2,JeanneB.Lawrence4, Melissa J. Moore3,DanielR.Caffrey1*andKatherineA.Fitzgerald1*, 1Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, 2School of Biochemistry and Immunology, Trinity College Dublin, Ireland, 3Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA, 4Department of Cell and Developmental Biology, University of Massachusetts Medical School, Worcester, MA

Sterile inflammation: Surface LIPIDS on STIMULATED T Cells that Induce Cytokine Production in HumanMonocytes/Macrophages, Paper 35Rakel Carpintero(1) , Isabelle Riezman(2),LyssiaGruaz(1),HowardRiezman(2),andDanielleBurger(1),(1)Division of Immunology and Allergy and (2)Department of Biochemistry, University of Geneva, Geneva, Switzerland



INTERNATIONAL CYTOKINE SOCIETY 9

Herpes Simplex Virus Type I Selectively Blocks Development of Neuronal Precursors Derived from Neural Progenitor Cell, Paper 36DanielCarr1, 2, Min Zheng1,ThomasE.Lane3, and Ana Chucair-Elliott1, 1Ophthalmology, 2Microbiology and Immunology, OUHSC, Oklahoma City, OK.; 3Department of Biochemistry, Univ. California-Irvine, Irvine, CA

Caspase-11 Controls Inflammasome Activation in Response to Bacterial Secretion Systems that Access the Host Cell Cytosol, Paper 37CierraN.Casson1, Alan M. Copenhaver1, Erin E. Zwack2,HieuT.Nguyen1,TillStrowig3, Bahar Javdan1, William P. Bradley1, ThomasC.Fung1, Richard A. Flavell3, Igor E. Brodsky2, and Sunny Shin1, 1Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA, 2Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA, 3Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut, USA

The Function of ADAM17 in Colitis-Associated Cancer, Paper 38Athena Chalaris-Rißmann1, Stefanie Schmidt1, Olga Will2, Philip Rosenstiel3, and Stefan-Rose-John1, 1Institute for Biochemistry, CAU, Kiel, Germany, 2Molecular Imaging North, UKSH, Kiel, Germany, 3Institute of Clinical Molecular Biology, CAU, Kiel, Germany

Differential Post-Translational Modifications Regulate Pathway-Specific Functions of IRF-3, Paper 39Saurabh Chattopadhyay, Ying Zhang and Ganes C. Sen, Department of Molecular Genetics, Lerner Research Institute, Cleveland, OH 44195

Myxomavirus-Derived Serpin Prolongs Survival and Reduces Vasculitis in Lethal Herpesviral Infection in Mice by Modulating Thrombotic Factor X and Inflammatory Cytokine IL-10, Paper 40HaoChen1,DonghangZheng1,LiyingLiu1, Mee Y Bartee1,JenniferDavids1, Colin Macaulay2, Jim Strong3,HeinzFeldmann3, Grant McFadden4,DavidA.Lomas5,HerbertW.Virgin6, and AlexandraLucas7,1Divisions of Cardiology and Rheumatology, Department of Medicine and Department of Molecular Genetics and Microbiology, and University of FL, Gainesville, FL USA, 2Viron Therapeutics, Inc, London, ON, Canada, 3National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba,Canada, (Present address - Laboratory of Virology, Division of Intramural Research (DIR), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Rocky Mountain Laboratories,Hamilton, Montana, USA), 4Department of Molecular Genetics and Microbiology, 5Division of Pulmonary Medicine,Department of Medicine, University of Cambridge, Cambridge, UK, 6Herbert W. Virgin –Departments of Pathology and Immunology and Molecular Microbiology, Washington University, St Louis MO, USA, and 7Divisions of Cardiology and Rheumatology, Department of Medicine and Department of Molecular Genetics and Microbiology, University of FL, Gainesville, FL USA

Changes in Plasma Cytokine Levels are Associated with Shockwave Treatments in Horses, Paper 41Jin-Wen JW Chen1, Cornelius C Uboh1,2, Mary M Robinson1, Zibin Z Jiang1,andLawrenceLSoma1, 1University of Pennsylvania School of Veterinary Medicine, New Bolton Center Campus, Kennett Square, PA, USA; 2Pennsylvania Equine Toxicology & Research Center, West Chester University, West Chester, PA, USA

Signal Relay by CCR2 and Formylpeptide Receptor-2 (Fpr2) in the Recruitment of Monocyte-Derived Dendritic Cells in Allergic Airway Inflammation, Paper 42KeqiangChen1,MingyongLiu1,YingLiu1, Chunyan Wang1,TeizoYoshimura1, Wanghua Gong2,YingyingLe3,LinoTessarollo4 and Ji Ming Wang1, 1Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, 2SAIC-Frederick, Frederick, MD 21702, 3Institute for Nutritional Sciences, Chinese Academy of Sciences, Shanghai 200031, China, 4Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick,MD 21702

Type I Interferon Promotes FLT3 Ligand-Dependent Plasmacytoid Dendritic Cell Development from Common Lymphoid Progenitor, Paper 43Yi-LingChen,Ting-TingChen and Chien-KuoLee , Graduate Institute of Immunology, National Taiwan University College of Medicine, Taipei 100, Taiwan


Monday, September 30, continuedP

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Interferon-Dependent Increase in STAT1, STAT2, and IRF9 Prolongs Resistance to Viruses and DNA Damage, Paper 44HyeonJooCheon,EliseG.Holvey-Bates,andGeorgeR.Stark,Department of Molecular Genetics, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA

The Novel PEGylated Interferon-Alpha (“Algeron”) Plus Ribavirin for Treatment of Chronic Hepatitis C Virus Infection: Results from a Phase II Study, Paper 45T.Chernovskaya1, R. Ivanov1,Yu.Linkova1, O. Znoyko2, M. Mayevskaya3 andE.Klimova2, 1Biopharmaceutical company “BIOCAD”; Russia, 2Moscow State University of Medicine and Dentistry named after A.I. Evdokimov; Russia, 3I.M. Sechenov First Moscow State Medical University, Russia

Reciprocal Interaction Between NK and DC Regulates the Autopathogenic Th17 Response by ControllingtheInnateIFN-γ/IL-27Axis, Paper 46WaiPoChong,JunChen,PhyllisBSilver,ReikoHorai,MaryJMattapallil,RuZhouandRachel R Caspi, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892-1857, USA

Proinflammatory Cytokines and Splanchnic Blood Flow in Acute Pancreatitis, Paper 47S. Chooklin and O. Usach, Medical University, Lviv, Ukraine

Immunophenotyping Innate Lymphoid and T Helper Cell Populations in Human Asthma, Paper 48LauraS.Christian1,LauraSimpson1, John Fahy2, Prescott Woodruff2,K.MarkAnsel1, 1Department of Microbiology & Immunology and Sandler Asthma Basic Research Center,2Department of Medicine, Division of Pulmonary and Critical Care Medicine and Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, USA

Excellent Antiviral and Antitumor Effect of the Super Interferon-I (sIFN-I), Paper 49LiangChu1,Kang-JiangZhang1, Guang-Wen Wei3andXin-YuanLiu1,2, 1Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences; 2Xin Yuan Institute of Medicine and Biotechnology, College of Life Science, Zhejiang Sci-Tech University; 3Hui-Yang Life Science and Technology Corp., Chengdu 610017, China

African Swine Fever Virus Include Multiple Mechanisms for the Manipulation of Interferon Responses, Paper 55S. Correia1, S. Ventura1, S. Goodbourn2 and RME Parkhouse1, 1 Instituto Gulbenkian de Ciência, Oeiras, Portugal, 2 Division of Basic Medical Sciences, St. George’s, University of London, Reino Unido

STAT-1 Regulates Constitutive and IL-6/PMA-Inducible MMP-1and MMP-3 Expression in Colorectal Cancer via Proximal Promoter STAT Binding Elements, Paper 56Samuel J. Cutler1,JamesD.Doecke1, Ibtisam Ghazawi1, Jinbo Yang2, Albert S. Mellick1,3 and Stephen J. Ralph1 , 1School of Medical Science and Genomics Research Centre, Griffith Institute of Health and Medical Research, Griffith University, Gold Coast Campus, Queensland, Australia, 2School of Life Science, Lanzhou University, Lanzhou, People’s Republic of China, 3Host response to cancer group, Griffith Institute of Health and Medical Research, Griffith University, Gold Coast Campus, Queensland, Australia

Evaluating Influences of Fructans on Cytokine and Immunoglobulin Production in a Human Clinical Trial, Paper 50SandraT.Clarke1,MartinKalmokoff2, Stephen P.J. Brooks3, Premysl Bercik4,DanRamdath5 and Julia M. Green-Johnson1, 1Applied Bioscience Graduate Program & Faculty of Science, University of Ontario Institute of Technology, Oshawa, Ontario, Canada, 2Atlantic Food and Horticulture Research Center, Agriculture and Agri-Food Canada, Kentville, Nova Scotia, Canada, 3Bureau of Nutritional Sciences, Health Canada, Ottawa, Ontario, Canada, 4Department of Medicine, McMaster University Medical Center, Hamilton, Ontario, Canada, 5Guelph Food Research Centre, Agriculture and Agri-Food Canada, Guelph, Ontario, Canada

Toll-Like Receptor Stimulated Macrophages Intrinsically Control Inflammatory Cytokine Production via CD39-Based Mechanism, Paper 51HeatherB.Cohen1,2,KatharineT.Briggs3, John P. Marino3,4,KatyaRavid5, Simon C. Robson6andDavidM.Mosser1 ,2, 1University of Maryland, College Park Department of Cell Biology and Molecular Genetics, College Park, MD, USA 2Maryland Pathogen Research Institute, College Park, MD, USA, 3Institute of Bioscience and Biotechnology Research, Rockville, MD, USA 4National Institute of Standards and Technology, Rockville, MD, USA 5Boston University, School of Medicine, Boston, MA, USA 6Harvard Medical School, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA

Programmed Cell Death 4 (PDCD4) Regulates Proinflammatory Cytokine Signaling in Bacterial Pneumonia, Paper 52TaylorS.Cohen and Alice Prince, Columbia University, New York, NY USA



Inhibition of Interleukin-15 Dependent Cytotoxic T-Cell Proliferation by the Action of Adenosine on Dendritic Cells, Paper 53YairCohen,HadarEini,CidioChaimovitz,andAmosDouvdevani. Department of Clinical Biochemistry and Pharmacology, Soroka Medical Center and Ben-Gurion University of the Negev, Beer-Sheva, Israel

Role of Transforming Growth Factor-Beta Signaling In CD8+ T Cells in Mucosal Anti-Viral Immune Responses, Paper 54BenjaminL.Cohn1,2, Joey Pham1andShomysehSanjabi1,2,1Gladstone Institute of Virology and Immunology, San Francisco, California, USA, 2Department of Microbiology and Immunology, University of California, San Francisco, California, USA

Pivotal Role of the IKK-Related Kinase IKK Epsilon to Modulate IL29 or type I IFN Induction during Hepatitis C Virus Infection, Paper 57StéphanieDabo1, Claire Gondeau2,MartineDaujat-Chavanieu2,DanielaBruni1,TakajiWakita3 and Eliane F. Meurs1, 1 Unit of Hepacivirus and Innate Immunity, Institut Pasteur, Paris, France, 2 INSERM U1040, Montpellier, France ;3 Department Virology National Institute of Infectious Diseases, Tokyo, Japan

IL-27 Inhibits HIV-1 Infection in Human Macrophages by Down-Regulating Host Factor SPTBN1 during Monocyte to Macrophage Differentiation, Paper 58LueDai1,KristyB.Lidie1, Qian Chen1, Joseph W. Adelsberger1, Xin Zheng1,DaWeiHuang1, Jun Yang1,RichardA.Lempicki1, TauseefRehman1,RobinL.Dewar1, Yanmei Wang1,RonaldL.Hornung1,KelseyA.Canizales1,StephenJ.Lockett2,H.CliffordLane3andTomozumiImamichi1 , 1Applied and Developmental Directorate, Science Applications International Corporation-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702,USA; 2Advanced Technology Program Directorate, Science Applications International Corporation-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA;3Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA

1,25(OH)2D3InhibitsTh17CytokineProductionandRORγtExpressionthroughGATA3/IL-4-Dependentand–IndependentMechanisms, Paper 59WendyDankers1,2,JanPietvanHamburg1,2, Anne-Marie M.C. Mus1,2,PatrickS.Asmawidjaja1,2,JohannesP.T.M.vanLeeuwen3,RudiW.Hendriks4,LouisBoon5, Edgar M. Colin1,6andErikLubberts1,2, Departments of 1Rheumatology, 2Immunology, 3Internal Medicine and 4Pulmonary Medicine, Erasmus MC University Medical Center, Rotterdam, The Netherlands, 5Bioceros, Utrecht, The Netherlands and 6Department of Rheumatology, ZGT, Almelo, The Netherlands

Oral Rapamycin Prevents Carcinogen-Induced Dermal Carcinogenesis through Immune Mechanisms, Paper 60VinhDao1,VincentHurez1,SriLakshmiPandeswara1,LishiSun1,AijieLiu1,PaulHasty2,DaveSharp2andTylerJ.Curiel1, 1Department of Medicine, and CTRC, University of Texas Health Science Center, San Antonio, TX, USA, 2Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX, USA

IL-20ReceptorSignalingInhibitsCutaneousIL-1βandIL-17AProductiontoPromoteMethicillin-ResistantStaphylococcus aureus Infection, Paper 61SandipDatta, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA

The Integrated Stress Response Regulates the Severity of DSS Colitis via Chop-Mediated Controlof Inflammatory Cytokine Gene Expression, Paper 62ShyamasreeDatta,NatalibethBarrera,PaulPavicicJr,ChenyangZhao,MichaelNovotny,andThomasHamilton, Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA

Investigating the Anti-Inflammatory Effects of HDL in Macrophages, Paper 63DominicDeNardo1*, LarisaLabzin1*,HajimeKono2, Reiko Seki2, Susanne Schmidt3, Johanna Vogelhuber1,MichaelKraut3, AnjaKerksiek4,WolfgangKrebs3,NiklasBode5, Alena Grebe1, Sebastian Zimmer5,ManfredKneilling6, Martin Röcken6,DieterLütjohann4,SamuelD.Wright7, Joachim Schultze3*andEickeLatz1,8,9* 1Institute of Innate Immunity, University Hospitals, Biomedical Centre, University of Bonn, Germany, 2Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan. 3Life and Medical Sciences Institute (LIMES), University of Bonn, Germay, 4Instititute for Clinical Chemistry and Clinical Pharmacology, University of Bonn, Germany, 5Department of Medicine/ Cardiology, University of Bonn, Germany, 6Department of Dermatology, Eberhard Karls University, Tuebingen, Germany, 7Cardiovascular Therapeutics, CSL Limited, Parkville, Australia, 8Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, USA, 9German Center for Neurodegenerative Diseases (DZNE, Bonn, Germany) * These authors contributed equally to this work.



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Transgenic Mice Carrying Interferon-Regulated Human MxA Locus are Highly Resistant to Avian but not Human Influenza A Viruses, Paper 64ChristophDeeg,PascalMutz,CarstenKallfass,CindyNürnberger,SébastienSoubiesandPeter Staeheli, Department of Virology and Institute of Medical Microbiology and Hygiene (IMMH), University of Freiburg Medical Center, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany

Production of CCL2 by Astrocytes in the Inflamed CNS Is Critical for the Development of EAE through the Recruitment of Myeloid Cells from the Periphery, Paper 65MonicaA.Delgado1,2,4, Joyce Ma2,4,EunyoungLee2,4, Erica McCauley4,LairdMiers4, Athena M. Soulika1,2,3,4,andDavidPleasure1, 2, 4, 1Department of Immunology, 2Department of Neurology, 3Department of Dermatology, 4Institute for Pediatric Regenerative Medicine, University of California, Davis, School of Medicine and Shriners Hospital for Children, Sacramento

Signal-Specific,Genome-WideRegulationofNuclearFactor-ΚappaBActivationbyEpidermalGrowthFactorandInterleukin-1, Paper 66JosephineKTDermawan1,2, and George R Stark2 , 1Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio USA, 2 Department of Molecular Genetics, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA

Assessmentofβ2-Adrenergic Receptors on Leukocyte Subpopulations Using Imaging Cytometry, Paper 67AlexPDiBattista1, Shawn G. Rhind2, Maria Y. Shiu1, Andrew Baker3,RuthA.Lanius4,DonaldJ.Richardson4,5 and Rakesh Jetly6,1Graduate Program, University of Toronto, Toronto, ON, Canada; 2Defence Research & Development (DRDC) Canada Toronto, Toronto, ON, Canada; 3Dept of Critical Care, Trauma & Neurosurgery Program, St. Michael’s Hospital, University of Toronto, Toronto, ON, Canada; 4Dept of Psychiatry, Schulich School of Medicine, Western University, London, ON, Canada; 5Parkwood Operational Stress Injury Clinic, St. Joseph’s Health Care, London, ON, Canada; 6Canadian Forces Health Services, Directorate of Mental Health, Dept of National Defence, Canada

MetabolismofDietaryFlavonoidsAlterstheirEffectonTumorNecrosisFactor-α, Paper 68J.L.diGesso1,2,J.S.Kerr1,2,S.K.Yalamanchili2, A. Cassidy1N.P.Botting3,D.O’Hagan3, Q. Zhang3, S. Raheen3, C.D.Kay1 and M.A. O’Connell2. 1Department of Nutrition, Norwich Medical School, University of East Anglia, Norwich, United Kingdom, 2School of Pharmacy, University of East Anglia, Norwich, United Kingdom, 3School of Chemistry, St. Andrews University, St. Andrews, United Kingdom

Interferon-Lambda is Produced by and Induces Autocrine Expression of Interferon-Stimulated Genes in Human Bronchial Epithelial Cells, Paper 69HaroldDickensheets1, Faruk Sheikh1, Rachel Shepard2,PhilippaHillyer2,RonaldL.Rabin2 and RaymondP.Donnelly1, 1Division of Therapeutic Proteins, Center for Drug Evaluation and Research, and 2Division of Bacterial, Parasitic and Allergenic Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, USA

Orchestration of Tissue Repair by the Humoral Pattern Recognition Molecule PTX3: Linking Microbe and Matrix Recognition, Paper 70A.Doni1, M. Sironi1,T.Musso2, C. Castagnoli2, M. Gobbi3, S. Valentino1,S.Tartari1, B. Bottazzi1, C. Garlanda1 and A. Mantovani1, 4,1Humanitas Clinical and Research Center, 2Dept. Public Health and Microbiology, University of Turin, Italy; 3Mario Negri Institute, Milan, Italy; 4Dept. Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy

Mechanisms of IL-23 Mediated Th17 Inflammation, Paper 71FangDu,AlyceMarsh,MatthewHenkel,LihuaMingandMandy J McGeachy, Division of Rheumatology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, 15261

EGR2 Is Critical for Peripheral Naïve T Cell Differentiation and the T-Cell Mediated Response to Influenza, Paper 72NingDu,Hyok-JoonKwon1,PengLi,JangsukOh,WeiLiao,andWarrenJ.Leonard,Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD ,1Current Address: Albert Einstein College of Medicine, New York, NY, USA



Regulation and Function of IL-1F11-Producing Lung Resident Cells, Paper 73ClaudiaU.Duerr1,2 andJörgH.Fritz1,2, 1Complex Traits Group, 2 Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada

IL-7R: Mutations in T-ALL and Polymorphisms in Autoimmunity, Paper 74ScottK.Durum1,W.Q.Li1, P. Zenatti2,D.Ribeiro3,L.Zuurbier 4, M. C. Silva3, M. Paganin5,J.Tritapoe1,J.A.Hixon1, A.B. Silveira2, B. A. Cardoso3,L.M.Sarmento3,N.Correia3,M.L.Toribio6,J.Kobarg7,M.Horstmann8,9, R. Pieters4, S.R. Brandalise2,10, A. A. Ferrando5,11,J.P.Meijerink4, J. A,Yunes2,12,andJ.T.Barata3, 1National Cancer Institute, USA;2 Centro Infantil Boldrini, Brazil; 3 Universidade de Lisboa, Portugal; 4 Erasmus Medical Center, The Netherlands; 5Columbia University, USA; 6Universidad Autónoma de Madrid, Spain; 7Centro Nacional de Pesquisa em Energia e Materiais, Brazil; 8German Cooperative Study Group for Childhood Acute Lymphoblastic Leukemia; 9University Medical Center Hamburg-Eppendorf, Germany; 10Universidade Estadual de Campinas, Brazil; 11 Columbia University USA; 12 Universidade Estadual de Campinas, Brazil

InterferonRegulatoryFactor4(IRF4)MediatesIFN-βandλ1ExpressionuponTLR4andMRChallengeinHumanAlternatively Activated Macrophages, Paper 75Ashraf El Fiky, RogerPerreault,GwendolynJ.McGinnis,andRonaldL.Rabin,Laboratory for Immunobiochemistry, Division of Bacterial, Parasitic and Allergenic Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, United States Food and Drug Administration, Bethesda, MD 2089

ADAM17 is Activated upon Cellular Senescence and Contributes to the Secretory Profile of Senescent Cells by Ectodomain Shedding, Paper 76TimoEffenberger,JanvonderHeyde,KareenBartsch,AthenaChalaris,StefanRose-JohnandBjörnRabe, Institute of Biochemistry, Medical Faculty, University of Kiel, Germany

The Immune System Cannot Generate Immunological Memory during Infection with the Lyme Disease Agent B. Burgdorfer, Paper 77R. A. Elsner,S.W.BartholdandN.Baumgarth,Graduate Group in Microbiology and the Center for Comparative Medicine, University of California-Davis, Davis, CA, USA

Therapeutic Inhibition of Gp130/Jak/Stat3-Dependent Cytokine Signaling Suppresses WNT-Dependent Colon Cancer Formation, Paper 78Matthias Ernst,TobyJ.Phesse,StefanThiemandMichaelBuchert,Cell Signaling and Cell Death Division The Walter and Eliza Hall Institute of Medical Research, Parkville VIC 3052, Australia

IL-6 Regulation of Th1 Responses Drives Fibrosis in Unresolved Inflammation, Paper 79Ceri A. Fielding1*, Gareth W. Jones1*,PhilipR.Taylor1, Brendan J. Jenkins2,NicholasTopley1, and Simon A Jones1, 1Cardiff Institute of Infection and Immunity, The School of Medicine, Cardiff University, Cardiff, Wales, UK, 2Centre for Innate Immunity and Infectious Diseases, Monash Institute for Medical Research, Monash University, Victoria, Australia, *Equal contributions

Novel Multi-Functional Drugs for the Treatment of Neurodegenerative Diseases, Paper 80Efrat Finkin-Groner1, Inessa Yanovsky2,AbrahamNudelman2 and Marta Weinstock1, 1Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel, 2Department of Chemistry Bar Ilan University Ramat Gan, Israel

Regulation of CD4 T Cell Derived IL-10 during Influenza Infection Paper 81NicoletteMFonseca,StephenARedpath,JungHeeSeoandGeorgiaPerona-Wright,Department of Microbiology and Immunology, University of British Columbia, Vancouver BC.

IL-36PromotesMyeloidCellInfiltration,ActivationandInflammatoryActivityinSkin, Paper 82Alexander M. Foster1, Jaymie Baliwag1, Cynthia S. Chen1, Andrew M. Guzman1, Stefan W. Stoll1,JohannE.Gudjonsson1, NicoleL.Ward2 and Andrew Johnston1,2Department of Dermatology, University of Michigan Medical School, Ann Arbor, Michigan,2 Department of Dermatology, Case Western Reserve University, Cleveland, Ohio



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AntiviralandImmunomodulatoryActivityofDifferentHumanInterferon-αSubtypesduringChronicViralInfections, Paper 83Sandra Francois1, Christopher Berendes1,MirkoTrilling1, Jacob Piehler2,UlfDittmer1, and KathrinGibbert1, 1 Institute of Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany,2Division of Biophysics, University of Osnabrück, Osnabrück, Germany

Extensive Collaboration of Immune Master Regulators IRF3 and NFκB in RNA Pol II Recruitment and Pause-Release in Human Innate Antiviral Transcription, Paper 84JonathanE.Freaney,RebeccaKim,andCurtM.Horvath,Department of Molecular Biosciences, Northwestern University, Evanston, IL 60201, USA

A Novel Role for the Oligoadenylate Synthetase-Like Protein in Viral Recognition and Interferon Induction, Paper 85HansHenrikGad1, Mikkel S. Ibsen1,LineL.Andersen1,VeitHornung2,SaumendraN.Sarka3,andRuneHartmann1, 1Aarhus University, Aarhus, Denmark, 2University Hospital of Bonn, Bonn, Nordrhein-Westfalen, Germany. 3University of Pittsburgh, Pittsburgh, Pennsylvania, USA

IFN-γ,ER-Stress,AutophagyandAntimicrobialDefense:ANovelATF6/C/EBP-β Centric Signaling Pathway, Paper 86PadmajaGade1, Srikatha Belagihalli1, Girish Ramachandran1, Alan S. Cross1,KazutoshiMori2, and Dhan V.Kalvakolanu1, 1Departments of Microbiology and Immunology; and Greenebaum Cancer, University of Maryland School of Medicine, Baltimore, MD 21201, USA, and 2Department of Biophysics, Kyoto University, Kyoto, Japan

Caspase-8Regulatesβ-GlucanInducedIL-1βProductionandCellDeath, Paper 87Sandhya Ganesan1,VijayA.K.Rathinam1,LukasBossaller1,WilliamJ.Kaiser2, Edward S. Mocarski2,DouglasR.Green3,NealS. Silverman1*andKatherineA.Fitzgerald1*, 1DepartmentofMedicine,UniversityofMassachusettsMedicalSchool,Worcester,MA, USA, 2DepartmentofMicrobiologyandImmunology,EmoryVaccineCenter,EmoryUniversitySchoolofMedicine,Atlanta,GA, USA, 3DepartmentofImmunology,St.JudeChildren’sResearchHospital,Memphis,TN,USA,*Theseauthorscontributedequallytothiswork.

CXCR3 Modulates CXCL12-Mediated Cellular Responses in Chronic Lymphocytic Leukemia, Paper 88Sylvia Ganghammer1,ElisabethHinterseer1,KarinJöhrer2, Richard Greil1, and TanjaNicoleHartmann1, 1 Laboratory for Immunological and Molecular Cancer Research, 3rd Medica Department with Hematology, Medical Oncology, Hemostasiology, Infectious Diseases, and Rheumatology, Paracelsus Medical University, Salzburg, Austria, 2Tyrolean Cancer Research Institute, Innsbruck, Austria

HighEfficiencyTargetingofInterferonαActivity, Paper 90Geneviève Garcin1, Franciane Paul1, Markus Staufenbiel2, Yann Bordat1,JoséVanderHeyden3, Stephan Wilmes2, Guillaume Cartron1,4, Florence Apparailly5,StefaanDeKoker6, Jacob Piehler2,JanTavernier3 and Gilles Uzé1, 1CNRS UMR 5235, Montpellier, France, 2Division of Biophysics, Department of Biology, University of Osnabrück, Osnabrück, Germany, 3Department of Medical Protein Research, Flanders Institute for Biotechnology, Ghent University, Faculty of Medicine and Health Sciences, Ghent, Belgium, 4Département d’Hématologie Clinique, CHU Montpellier, Montpellier, France, 5INSERM U844, Montpellier, France, 6Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium

Homotypic T-T Synapses Promote Collective CD8+ T Cell Differentiation through Exchange of IFN gamma, Paper 91Audrey Gérard1,OmarKhan1, Peter Beemiller1, Erin Oswald1,JoyceHu2, Mehrdad Matloubian2andMatthewF.Krummel1, 1 Department of Pathology and 2Division of Rheumatology, Department of Medicine, University of California San Francisco, San Francisco, USA

STAT5 Activates the C-Mycproximal Promoter: Elevated STAT5 or C-Myc Expression Relative to STAT1 is Linked with ReducedSurvivalofMelanomaPatientsGivenIFNγTherapy, Paper 92Ibtisam Ghazawi1, Albert S. Mellick1, Samuel J. Cutler1,JamesDoecke2, Jeanette Raleigh3, Grant McArthur3,4,5

and Stephen J. Ralph1, 1School of Medical Science and Griffith Health Institute, Griffith University, Southport, Qld, 4222 Australia; 2CMIS, Royal Brisbane Women’s Hospital, Herston, Brisbane, Australia;3Division of Cancer Medicine and Research, Peter MacCallum Cancer Centre, EastMelbourne, Vic., Australia; 4Department of Pathology, University of Melbourne, Parkville, Victoria, Australia; 5Department of Medicine, St Vincent’s Hospital, University of Melbourne, Fitzroy, Victoria, Australia



Role of Cytokines in the Natural Resistance of Baboons to SIV Infection, Paper 93LuisD.Giavedoni1,2,LauraM.Parodi1,2, Veronica Obregon-Perko1,LisaM.Smith1, Jessica Callery1,andVidaL.Hodara1,2, 1Department of Virology & Immunology, 2Southwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA

Interleukin-22 Mediates Protection during a Murine Model of Cutaneous Leishmaniasis, Paper 94Ciara Gimblet1,DavidArtis2 and Phillip Scott1, 1Department of Pathobiology, University of Pennsylvania, Philadelphia, PA, USA, 2Department of Microbiology, University of Pennsylvania, Philadelphia, PA, USA

Type I Interferon Regulates Acute IL-5 and IL-13 Expression in Human Memory CD4+ T Cells, Paper 95SarahR.Gonzales-vanHorn,JonathanP.HuberandJ.DavidFarrar,Department of Immunology, UT Southwestern Medical Center, Dallas, Texas USA

Evolutionary Conservation of STING, an Innate Immune Effector and DNA Sensor, in Drosophila Melanogaster, Paper 96Alan G. Goodman1,BrandonM.Kitay2,KeikoKonno1, R. Grace Zhai2andGlenN.Barber1, 1Department of Cell Biology, 2Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, Florida, USA

Silencing MicroRNA-21 Ameliorates Th17 Mediated Autoimmune Inflammation, Paper 97Murugaiyan Gopal,AndrePiresdaCunhaandHowardL.Weiner,Center for Neurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA

Common Genetic Polymorphisms in the ST2 Gene Locus are Associated with Impaired Soluble ST2 Expression in the Airway Epithelium, Paper 98ErinDGordon1, Cydney Urbanek2, Shaopeng Yuan1, Prescott Woodruff1, John V Fahy1* and Max A Seibold2*,1Department of Medicine, University of California, San Francisco, San Francisco, California, 2Department of Pediatrics; National Jewish Health, Denver, Colorado, *Authors contributed equally.

IL-33 Splice Variants are Critical to its Regulated Secretion from Airway Epithelial Cells, Paper 99ErinDGordon1,MarrahLachowicz-Scroggins1, Cydney Urbanek2, Max A Seibold2*and John V Fahy1*1Department of Medicine, University of California, San Francisco, San Francisco, California and 2Department of Pediatrics; National Jewish Health, Denver, Colorado, *Authors contributed equally

Mitochondrial STAT3 Supports K-Ras Driven Myeloid Leukaemia in vivo, Paper 100Daniel.J.Gough1,2andDavid.E.Levy*1, 1 New York University Langone School of Medicine, 550 First Avenue, New York, NY, USA. 10016, 2 Present address: Monash Institute of Medical Research, 27-31 Wright St, Clayton, Victoria, Australia, 3168

Characterization of the Interferon Alpha Inducible protein LY6E, Paper 101DanielS.Green1, Joseph Bekisz1,MichaelDolan2andKathrynC.Zoon1, 1Cytokine Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD and 2Bioinformatics & Computational Bioscience Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

Interleukin 10 Control of the Inflammasome Restricts Arthritic Bone Erosion, Paper 102C.J. Greenhill1, G.W. Jones1, M.A.Nowell1,A.K.Harvey1,A.N.Moideen1,F.L.Collins1, A.C. Bloom1, R. Coll2, M. Rosas1, P.R. Taylor1,L.A.O’Neill2,I.R.Humphreys1, A.S. Williams1 and S.A. Jones1, 1Cardiff Institute of Infection & Immunity, The School of Medicine, Cardiff University, Wales, UK, 2Trinity Biomedical Sciences Institute, School of Biochemistry and Immunology, Trinity College Dublin, Ireland

Virulent Francisella tularensis do not Induce Arginase as a Mechanism of Virulence, Paper 103Amanda J. Griffin,DebbieD.Crane,TaraD.Wehrly,andCatharineM.Bosio,Immunity to Pulmonary Pathogens Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases/National Institutes of Health, Hamilton, MT, 59840, USA

The Structure of Human Interleukin-11 Reveals Features of Biological Significance, Paper 104MichaelD.W.Griffin1, Matthias Ernst2andTracyL.Putoczki2, 1Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Victoria, Australia, 2The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia



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Expression of the Strawberry Notch 2 Gene is Altered in the Murine Brain Following LPS-Endotoxemia and Viral Infection, Paper 105Magdalena Grill1,AlineL.Noçon1,WenLi1, Stefan Rose-John2andIainL.Campbell1, 1School of Molecular Bioscience, University of Sydney, Sydney, Australia and 2Department of Biochemistry, University of Kiel, Kiel, Germany

Critical Role for the 3’UTR in the Post-Transcriptional Regulation of the Gene Encoding the Key Inflammasome Protein NLRP3, Paper 111MoritzHaneklaus1,SethL.Masters2 andLukeA.J.O’Neill1, 1Inflammation research group and Immunology Research Centre, School of Biochemistry and Immunology, Trinity College Dublin, Ireland, 2The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia

Lactococcus lactis Expressing IL-27: A Potential Therapeutic for Inflammatory Bowel Disease, Paper 112MirandaL.Hanson,1,JulieA.Hixon1,WenqingLi1,BarbaraK.Felber2, Miriam R. AnverR3, Charles A. Stewart1, Wei Shen1, Mairi McLean1, Pieter Rottiers4,LotharSteidler4 andScottK.Durum1 1Cancer Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, 2Human Retrovirus Pathogenesis Section, Vaccine Branch, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, 3Laboratory Animal Services Program, Science Applications International Corporation, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, 4ActoGenix N.V., Zwijnaarde, Belgium

Type I Interferon Signaling is Suppressed in Experimental Autoimmune Encephalomyelitis (EAE): Implications for Multiple Sclerosis, Paper 113DanielHarari1 , Renne Abramovich 1,NadineKallweit2, Sandrine Pouly 4, Alla Zozulya-Weidenfeller 3, Paul Smith 3, Martin Schlapschy 2,MarioKöster 5,HansjörgHauser 5 Arne Skerra2 and Gideon Schreiber1,1Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel, 2Lehrstuhl für Biologische Chemie,Technische Universitaet Muenchen, Freising-Weihenstephan, Germany, 3,4MS Platform – Research 3 or 4 MS Pharmacology & Early PK/PD,TA Neurodegenerative Diseases, Merck-Serono S.A., Geneva, Switzerland 5Helmholtz Centre for Infection Research, Dept. Gene Regulation and Differentiation, Braunschweig, Germany.

Tuesday, October 1, 2013

8.30 – 10:30 am PLENARY SESSION II: Cytokines – Basic Mechanisms Grand Ballroom Chairs: Lewis Lanier, University of California, San Francisco, CA, USA and Keiko Ozato,NICHD,NIH,Bethesda,MD,USA

8:30 – 9:00 am Lymphocytes, Identity and Cytokines John O’Shea, NationalInstitutesofHealth,Bethesda,MD,USA

9:00 – 9:30 am Natural Killer Cell Memory – Role of Cytokines and Co-Stimulatory Receptors, Paper S-27 LewisLanier,UCSF,SanFrancisco,CA,USA

9 :30 – 10:00 am Transcriptional Cascades Associated with Inflammatory and Innate Immune Responses, Paper S-13 StephenSmale,UniversityofCalifornia,LosAngeles,CA,USA

10:00 – 10:30 am Compartmentalized and Systemic Control of Tissue Immunity by Commensals, Paper S-14 YasmineBelkaid,NationalInstituteofAllergyandInfectiousDiseases,NIH,Bethesda,MD,USA

10:30 – 11:00 am Coffee Break - visit with the exhibitors Pacific Concourse


SYMPOSIUM T3: T Cell Subsets Grand Ballroom A Chairs: Daniel Cua,MerckResearchLaboratories,PaloAlto,CA,USAand Amy Weinmann, University of Washington, Seattle, WA, USA



11:00 – 11:30 am Cytokine Function-Marking: Who Makes What? RichardLocksley,UniversityofCalifornia,SanFrancisco,CA,USA

11:30 – 12:00 pm TheIL-23PathwayinIntestinalInflammationandColonCancer FionaPowrie,UniversityofOxford,Oxford,UnitedKingdom

12:00-12:30 pm Differentiation and Function of Follicular Helper T Cells (Tfh), Paper S-4 ShaneCrotty,LaJollaInstituteforAllergyandImmunology,LaJolla,CA,USA


11:00 am – 1:30 pm SYMPOSIUM T4: Interferons Grand B/C Chairs: Bryan Williams, Monash Institute of Medical Research, Clayton, Victoria, Australia and Karen Mossman, McMaster University,Toronto,Ontario,Canada

11:00 – 11:30 am Role of PYHIN Proteins in Innate DNA Sensing and Gene Regulation, Paper S-2 Andrew Bowie, TrinityBiomedicalSciencesInstitute,TrinityCollege,Dublin,Ireland

11:30am–12:00N Innate DNA Sensing and IFN Induction during Viral Infections, Paper S-15 SørenPaludan,AarhusUniversity,Aarhus,Denmark

12:00 – 12:30 pm IL-1/Type I IFN Cross-Talk in Tuberculosis AlanSher,NationalInstitutesofAllergyandInfectiousDiseases,NIH,Bethesda,MD,USA

12:30 – 1:00 pm Novel Interferon and Interferon-Independent Signaling Pathways, Paper S-6 KarenLMossman


1:00 – 2:00 pm JICR EDITORIAL BOARD LUNCHEON Seacliff


MINISYMPOSIUM 3 Grand Ballroom A Chairs: Dhan Kalvakolanu, University of Maryland School of Medicine,Baltimore,MDUSAandLaurel Lenz,UniversityofColorado,Denver,COUSA

2:00 – 2:15 pm Critical Role for the 3’UTR in the Post-Transcriptional Regulation of the Gene Encoding the Key Inflammasome Protein NLRP3, paper 111 MoritzHaneklaus.SchoolofBiochemistryandImmunology,TrinityCollegeDublin,Ireland

2:15 - 2:30 pm The Interleukin-17-Mediated Regulation and Role of Neutrophils in Resistance to Oropharyngeal Candidiasis, Paper 124 AnnaHuppler,Children’sHospitalofPittsburghandUniversityofPittsburgh,Pittsburgh,PA,USA

ICIS POSTDOCTORAL INVESTIGATOR AWARD, 2nd Place2:30 – 2:45 pm Interleukin-27 as a Novel Antagonist of Ectopic Lymphoid-Like Structure Development in Early Inflammatory Arthritis, Paper 134 GarethJones,CardiffUniversity,Cardiff,UnitedKingdom


Tuesday, October 1, continued

2:45 – 3:00 pm Cytokine-Induced Tumor Suppressors: A GRIM Checkmates ST, Paper 137 DhanKalvakolanu

3:15 – 3:30 pm A Mechanism for the Anti-Inflammatory Effects of Type I IFNs in Myeloid Cells, Paper 142 LaurelLenz

MILSTEIN YOUNG INVESTIGATOR AWARD3:15 – 3:30 pm IRF8 and IRF1: Genomic Regulators of Innate Immunity, Paper 155 DavidLanglais,McGillUniversity,Montreal,Canada


MINISYMPOSIUM 4 Grand B/C Chairs: Keiko Ozato,NationalInstitutesofHealth,Bethesda,MarylandUSAand Yueh-Ming Loo, University of Washington, Seattle, WA, USA

2:00 - 2:15 pm The Role of Interferon Epsilon in the Immune Response in the Female Reproductive Tract, Paper 175 NiamhMangan,MonashUniversity,Victoria,Australia

HERBERT TABOR AWARD2:15 - 2:30 pm Identification and Characterization of Interferon-λ4 (IFN-λ4), A Novel Class-2 Cytokine which Impairs Clearance of Hepatitis C Virus, Paper 182 LudmilaProkunina-Olsson,NationalInstitutesofHealth,Bethesda,MD,USA

2:30 – 2:45 pm IRF8 Regulates Autophagy and Activates Microglia to Exacerbate Neuroinflammation, Paper 194

ICIS POSTDOCTORAL INVESTIGATOR AWARD, Co-1st Place2:45 – 3:00 Interleukin-7-Mediated NFAT Activation Sets the Threshold for T Cell Development, Paper 196 Amiya Patra. University of Würzburg, Würzburg, Germany

3:00 – 3:15 pm Interleukin-1 Drives Hematopoietic Stem Cell Differentiation and Myelopoiesis via a Pu.1-Dependent Molecular Program, Paper 198 Eric Pietras, University of California San Francisco, California USA

MILSTEIN YOUNG INVESTIGATOR AWARD3:15 – 3:30 pm The Convergence of IL-1 and Type I IFN on Antiviral Gene Networks is Regulated by Distinct IRF Family Member Cross-Talk, Paper 205 HilarioRamos,UniversityofWashingtonSchoolofMedicine,Seattle,WA,USA

3:30 – 4:00 pm Coffee Break - visit with the exhibitors Pacific Concoursev4:00 – 6:00 pm CONCURRENT SYMPOSIA

SYMPOSIUM T5: Autoimmunity Grand Ballroom A Chairs: Nancy Ruddle,YaleUniversity,NewHaven, CT,USAandBetsy Barnes,RutgersBiomedicalHealthSciences,Newark,NJ,USA

4:00 – 4:30 pm Cytokine Control of Regulatory B10 Cell Function, Paper S-16 ThomasTedder,DukeUniversityMedicalCenter,Durham,NC,USA



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4:30 – 5:00 pm The Regulation and Function of Interleukin-22 in Epithelial Homeostasis and Host Defense, Paper S-17 WenjungOuyang,Genentech,SouthSanFrancisco,CA,USA

5:00 – 5:30 pm Interferon Responses during the Initial Stages of Diabetic Autoimmunity EmilUnanue,WashingtonUniversity,St.Louis,MO,USA

5:30 – 6:00 pm Cytokines: Role in Induction of Regulatory B Cells (Breg) and Suppression of CNS Auto immune Disease, Paper S-18 CharlesEgwuagu,NationalEyeInstitute, NIH,Bethesda,MD,USA

4:00 – 6:00 pm SYMPOSIUM T6: Chemokines and their Receptors Grand B/C Chairs: Federica Sallusto, Institute for Research in Biomedicine, Bellinzona, Switzerland and Albert Zlotnik, University of California, Irvine, CA, USA

4:00 – 4:30 pm Oxysterols in Immune Cell Guidance and Regulation, Jason Cyster, University of California, San Francisco, CA, USA

4:30 – 5:00 pm T Cell Activation, Differentiation and Plasticity in Humans, Paper S-19 Federica Sallusto

5:00 – 5:30 pm Cellular Stress Selectively Amplifies TLR-Simulated Neutrophil Chemoattractant Expression TomHamilton,ClevelandClinic,Cleveland,OH,USA

5:30 – 6:00 pm Novel Genes Associated with the Immune System Albert Zlotnik

7:30 – 9:00 pm SPECIAL NETWORKING RECEPTION FOR STUDENTS, Seacliff A&B POSTDOCS AND NEW (1ST YEAR) FACULTY (Tickets Required) Sponsored by eBioscience

6:00 – 7:30 pm POSTER SESSION II (with wine and cheese) Pacific Concourse Papers: 114–139, 141-226

Interferon-Alpha Therapy Enhances the Anti-Friend Virus B Cell Response through Apobec3, Paper 114MichaelS.Harper1 , Bradley S. Barrett1,DianaS.Smith1,KarlJ.Heilman1,SamX.Li1,UlfDittmer2,KimJ.Hasenkrug3 and MarioL.Santiago1, 1Division of Infectious Diseases, University of Colorado Denver, Aurora, CO, 2University of Duisburg-Essen, Germany, 3Rocky Mountain Laboratories, NIAID,Hamilton, MT

Interleukin-10 Dependent Alterations in the Hypothalamic-Pituitary-Adrenal Axis and Behavior during Inflammatory Arthritis, Paper 115AnnK.Harvey1, Claire J. Greenhill1,MichaelJ.Newton2,MariahJ.Lelos2,StephenB.Dunnett2, Anwen S. Williams1,SeanL.Wyatt2, and Simon A. Jones1, 1Institute of Infection & Immunity, School of Medicine, Cardiff University, Cardiff, UK, 2School of Biosciences, Cardiff University, Cardiff, UK

No Significant Re-Directed CD8 nTreg Developed in Helper Deficient Mice, Paper 116XiaoHe,HuDaiandPeterEJensen,Department of Pathology, University of Utah, Salt Lake City, Utah, USA

Toll-Like Receptor and RIG-I Like Helicase Crosstalk is Essential to Protect against Lethal Infectionwith Vesicular Stomatitis Virus, Paper 117JuliaHeinrich1,DarrenBaker2, Gerd Sutter3,andUlrichKalinke1, 1Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, Hannover, Germany, 2BiogenIdec Inc., Cambridge, Massachusetts, USA, 3Institute for Infectious Diseases and Zoonosis, Ludwig-Maximilians University, Munich, Germany



Modulation of Treg and Th17 Fate Decision by Selective Ikaros Zinc Fingers, Paper 118 JenniferHeller1,HildeSchjerven2, Ju Qiu1,AileenLee1, Stephen Smale2, and LiangZhou1, 1 Microbiology & Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States, 2Microbiology, Immunology, & Molecular Genetics, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States

Interleukin-22 Protects against Intestinal Viral Infection through Enhancement of Interferon-λ Signaling Pathway, Paper 119PedroP.Hernandez1,3,TanelMahlakoiv2,NamNguyen1, Peter Staeheli2andAndreasDiefenbach1, 1Institute of Medical Microbiology and Hygiene, 2Department of Virology, University of Freiburg, and 3International Max Planck Research School for Molecular and Cell Biology (IMPRS-MCB), Freiburg,Germany

Loss of IFN-gamma 3’Untranslated Region AU-Rich Element Affects B220+ Cell Populations in Novel Murine Lupus Model, Paper 120DeborahL.Hodge1, Cyril Berthet2, Vincenzo Coppola3,HidekazuShirota1,DellaReynolds1, Michael Sanford1,FanchingLin1,DennisM.Klinman1 andHowardA.Young1, 1Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, MD USA 21702-1201, 2Oncodesign, 20 Rue Jean Mazen, Dijon, France, 3Department of Molecular Virology, Immunology and Medical Genetics Ohio State University 460 W.12th Street, Columbus, OH 43210

The Molecular Basis for the Differential Response of Astrocytes and Microglia to Oncostatin M, Paper 121Meng-PingHsu1, Ricardo Frausto1, Stefan Rose-John2,andIainLCampbell1, 1School of Molecular Bioscience, University of Sydney, Sydney, NSW, Australia and 2Department of Biochemistry, University of Kiel, Germany

Regulation of Thymocyte Development by Protein Phosphatase 4, Paper 122Ching-YuHuang,En-WeiHsing,Fang-HsueanLiao,Wan-IHsou,Yu-JunLin,andYi-JyunJhou,Immunology Research Center, National Health Research Institutes, Zhunan, Miaoli County, 350, Taiwan

IL-33 Drives Biphasic IL-13 Production for Noncanonical Type 2 Immunity against Hookworms, Paper 123Li-YinHung1,4,IanP.Lewkowich2,4,LucasA.Dawson2,JordanDowney2, Yanfen Yang2,DirkE.Smith3,andDe’BroskiR.Herberta1, 1Division of Experimental Medicine, University of California, San Francisco, CA 94110; 2Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229; and 3Department of Inflammation Research, Amgen, Seattle, WA 91320, 4L.-Y.H. and I.P.L. contributed equally to this work

The Interleukin-17-Mediated Regulation and Role of Neutrophils in Resistance to Oropharyngeal Candidiasis, Paper 124AnnaR.Huppler 1,2,NydiarisHernández-Santos 2,HeatherR.Conti 2andSarahL.Gaffen 2, 1Department of Pediatrics, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, USA, 2Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pennsylvania,USA

The Sin3a Repressor Complex Regulates the Balance between the Activities of Different STAT Proteins, Paper 125L.Icardi1, R. Mori1, V. Gesellchen1, S. Eyckerman1, J. Verhelst2,K.Vercauteren3, X. Saelens2, P. Meuleman3,K.DeBosscher1, M. Boutros4andJ.Tavernier1 ,1 Department of Medical Protein Research, VIB, 9000 Ghent, Belgium, 2Department of Molecular Biomedical Research, VIB, 9000 Ghent, Belgium, 3Center for Vaccinology, Ghent University and Hospital, Ghent University, 9000 Ghent, Belgium,4German Cancer Research Center (DKFZ), Department of Cell and Molecular Biology, Heidelberg, Germany

NOD1-Dependent Sensing of Bacterial Outer Membrane Vesicles and Induction of an Autophagic Response, Paper 126Aaron Irving1,LorindaTurner2,HitomiMimuro3, Chihiro Sasakawa3,ThomasKufer4,DanaPhilpott5, Richard Ferrero2 and Maria Kaparakis-Liaskos2, 1Centre for Cancer Research, Monash Institute of Medical Research, Clayton, Monash University, Victoria, Australia,2Centre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Clayton, Victoria, Australia,3Department of Microbiology and Immunology; Institute of Medical Science, University of Tokyo, Tokyo, Japan, 4Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Germany5,, Department of Immunology, The University of Toronto, Ontario, Canada

Role of TGF-Beta Signaling in Circulating and Tissue Resident Memory CD8+ T Cells, Paper 127HarumichiIshigame1,ShomysehSanjabi2, 3, and Richard A. Flavell1, 4, 1 Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA, 2 Gladstone Institutes, San Francisco, California, USA, 3 Department of Microbiology and Immunology, University of California, San Francisco, California, USA, 4 Howard Hughes Medical Institute



Truncated Form of Transforming Growth Factor-β Receptor II, but not its Absence, Induces Memory CD8+ T Cell Expansion and Lymphoproliferative Disorder in Mice, Paper 128HarumichiIshigame1, Munir M. Mosaheb1, 2, ShomysehSanjabi3, 4, and Richard A. Flavell1, 5, 1Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA,2Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA, 3Gladstone Institute of Virology and Immunology, San Francisco, California, USA, 4Department of Microbiology and Immunology, University of California, San Francisco, California, USA 5Howard Hughes Medical Institute

IFN-g and TNF Alter Epigenetic Landscapes to Control TLR-Induced Transcriptional Responses in Macrophages, Paper 129LionelB.Ivashkiv, Hospital for Special Surgery, Weill Cornell Medical College, New York, NY,USAvInterplay Between Epigenetic Mechanisms and Signaling Pathways Will Determine MacrophagePhenotypes in Response to Environmental Cues, Paper 130Sophia S. Jeon1,2andRobertL.Hendricks1,3,4 , 1Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; 2Graduate Program in Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; 3Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; and 4Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

Suppression of Antiviral Innate Immunity by Sunitinib Enhances Oncolytic Virotherapy, Paper 131BabalKantJha,BeihuaDong,IrinaPolyakova,andRobertH.Silverman,Department of Cancer Biology, Lerner Research Institute Cleveland Clinic, Cleveland, OH, USA

Sensing of DNA by Innate Immune Receptors, Paper 132TengchuanJin,JianshengJiang,PatrickSmith,andTsanSamXiao ,Structural Immunobiology Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA

In Vitro EradicationofSerousOvarianCancerwithIFN-α2αandIFN-γinCombinationwithMonocytes, Paper 133ChaseL.Johnson,DanielS.Green,JosephBekisz,andKathrynC.Zoon,Cytokine Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

Interleukin-27 as a Novel Antagonist of Ectopic Lymphoid-Like Structure Development in Early Inflammatory Arthritis, Paper 134Gareth W. Jones1, Michele Bombardieri2, Claire J. Greenhill1,LouiseMcLeod3, Vidalba Rocher2, Anwen S. Williams1, Costantino Pitzalis2, Brendan J. Jenkins3 and Simon A. Jones1, 1Institute of Infection & Immunity, School of Medicine, Cardiff University, Cardiff, UK, 2Centre for Experimental Medicine & Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, London, UK, 3Centre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Melbourne, Australia

Values of TNF Alpha in Cystic Fluid in Odontogenic Tumor Depending on Macrophage Number in Cystic Wall, Paper 135Vladimir Jurisic 1,T.Terzic2, M. Jurisic3, 1University of Kragujevac, Faculty of Medical Sciences, Kragujevac, Serbia, 2University of Belgrade, School of Medicine, Serbia, 3University of Belgrade, School of Dentistry, Belgrade, Serbia

Signal Transducer and Activator of Transcription 3 Induction and Function in NK Cells during Murine Cytomegalovirus Infection, Paper 136LaraE.Kallal and Christine A. Biron, Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI USA

Cytokine-Induced Tumor Suppressors: A GRIM Checkmates ST, Paper 137DhanV.Kalvakolanu1,SudhakarKalakonda1,ShreeramC.Nallar1andDanielJLindner2, 1 ,Department of Microbiology & Immunology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD, 2Taussig Cancer Center, Cleveland Clinic Foundation, Cleveland,OH, USA


Tuesday, October 1, continuedP

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A Fullerene Derivative, Bis-Malonic Acid Fullerene Inhibits IL-33-Induced InflammatoryCytokines via IKKb-Specific Pathway, Paper 138TadashiKasahara,YurikaMiyagawa,KazuhiOkamoto,TadahikoMashino,andMegumiFunakoshi-Tago,Keio University Faculty of Pharmacy, Shibakoen, Minato-ku, Tokyo, Japan, 105-8512

Tumors Selectively Eliminate Cancer Cells Incapable of Downregulating Type I Interferon Receptor, Paper 139KanstantsinV.Katlinski, Sabyasachi Bhattacharya and Serge Y. Fuchs, Department of Animal Biology, Mari Lowe Comparative Oncology Center, University of Pennsylvania, Philadelphia, PA 19104, USA

A Beneficial Effect of Type I Interferon Signaling in T Cells in the Early Phase of Experimental Autoimmune Encephalomyelitis (EAE), Paper 141NadiaKavrochorianou1,2, Melina Markogiannaki1,2,GeorgeThyphronitis2,andSylvaHaralambous1, 1Laboratory of Transgenic Technology, Hellenic Pasteur Institute, Athens, Greece, 2Department of Biological Applications and Technologies, University of Ioannina, Ioannina, Greece

A Mechanism for the Anti-Inflammatory Effects of Type I IFNs in Myeloid Cells, Paper 142StaciJ.Kearney1,2,ChristineDelgado2, Emily M. Eshleman2,KristaK.Hill1, Brian P. O’Connor1,3, and LaurelL.Lenz1,2, 1Integrated DepartmentofImmunology,NationalJewishHealth,Denver,CO80206,2IntegratedDepartmentofImmunology,UniversityofColorado,Denver,CO80045,3IntegratedCenterforGenes,EnvironmentandHealth,NationalJewishHealth,Denver,CO80045

Cytokine Patterns Associated with Persistent Inflammation or Viremic Control in HIV Infection, Paper 143SheilaM.Keating1 ,2 ,Evan Jacobs1, Busola Adesina1,ShiquanWu1,ElizabethT.Golub5,JohnW.Heitman1,MarekNowicki6, Maria Villacres6, Mary Young7,KathrynAnastos8,HowardCrystal9,StevenG.Deeks4,JeffN.Martin4, Jinbing Zhang3, Ruth M. Greenblatt3, AlanL.Landay10,PhilipJ.Norris1,2,4,andtheWomen’sInteragencyHIVStudy,1Blood Systems Research Institute, San Francisco, CA, 2Department of Laboratory Medicine, UCSF, San Francisco, CA, US, 3 Department of Pharmacology, UCSF, San Francisco, CA, US, 4Department of Medicine, UCSF, San Francisco, CA,US, 5Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, US, 6Department of Medicine, University of Southern California, Los Angeles, CA, US 7, Department of Medicine, Georgetown, Washington, DC, US, 8Departments of Medicine and Epidemiology & Population Health, Albert Einstein College of Medicine, Bronx, NY,US, 9Department of Medicine, SUNY Downstate,Brooklyn, NY, US, 10Department of Immunology/ Microbiology, RUSH University Medical Center, Chicago, IL, US

Receptor Occupancy and Internalization of an Anti-IL-7 Receptor Antibody, Paper 144BrentKern1,EugeniaKraynov1,Li-FenLee2,and Chad Ray 1, 1Pharmacokinetics, Dynamics, and Metabolism, Pfizer, La Jolla, California, USA, 2Experimental Medicine, Pfizer, San Francisco, California, USA

The Erthyrocyte Cytosolic 5’-Nucleotidase III is a Broad Tissue IFN-Stimulated Gene That Limits NF-κB-Mediated Inflammatory Response, Paper 145LatifaAl-HajandKhalidS.A.Khabar,Molecular BioMedicine Program, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia

Compression Force Induces Inflammatory Cytokines via Notch Signaling In Periodontal Ligament Cells, Paper 146JunKikuta,MasaruYamaguchi,KunihikoYamada,MamiShimizu,MariFunakoshiandKazutakaKasai,Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan

Proatherogenic Conditions Promote Autoimmune Th17 Responses in vivo, Paper 147YoungUkKim,1,2HoyongLim,1HuaSun,1ShinoHanabuchi,3Joseph M Reynolds3BabieTeng1,2 and Yeonseok Chung,1,2, 1Institute of Molecular Medicine, University of Texas Medical School at Houston, Houston, TX, USA, 2 Graduate School of Biomedical Sciences, the University of Texas Health Science Center at Houston, Houston, TX, USA,3Immunology, MD Anderson Cancer Center, Houston, TX, USA

Modulation of Cytokine Activity through Advanced Polymer Conjugation, Paper 148PeterKirk,MuraliAddepalli,CherieAli,ThomasChang,JicaiHuang,SteveLee,PaulSims,LaurieVanderVeen,YujunWangandDeborahCharych,Nektar Therapeutics, San Francisco, California, USA



Cell Crowding Results in Accumulation of Interferon-Stimulated Genes Independently of STAT1, Paper 149IrynaKolosenko1, Elin Edsbäcker1, Mårten Fryknäs2, Per Johnsson1,DanGrandér1,KatjaPokrovskajaTamm1,StigLinder1 and AngeloDeMilito1, 1 Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden, 2Division of Clinical Pharmacology, Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden

Physico-Chemical Properties, Pharmacokinetics and Pharmacodynamics of Pegylated Cytokines, Paper 150 D.Korzhavin1, E. Rudenko2, E. Morozova2andT.Chernovskaya2, 1Lomonosov Moscow University of Fine Chemical Technology, Russia, 2 Biopharmaceutical company “BIOCAD”, RussiaCXCR3 Deficient Mice are Resistant to Herpes Simplex Virus Type 1 Infection Associated with a Drop in Viral Titer in the Ependymal Region of the Brain,Paper 151ChandraKroll1, Min Zheng2,andDanielJ.J.Carr1,2, Departments of 1Microbiology, Immunology, and 2Ophthalmology OUHSC, Oklahoma City, OK

STAT4 Negatively Regulate Hepatocyte Survival during Auto-Immune Liver Inflammation,Paper 152Pawan Kumar, Kong Chen, Xuejun Zhao, Derek Pociask and Jay K. Kolls, Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA 15224

HMGB1 and TNF-Alpha in an Experimental Model of Acute Lung Injury (ALI) Under Protective Conventional Mechanical Ventilation (CMV), Paper 153CilmerySuemiKurokawa1, José Roberto Fioretto1JoãoPessoadeAraújoJúnior2, Rafaelle Batistella Pires1, Marcos A Moraes1, SusianeOKlefens1, Maria Regina Moretto1,CristinaMariaTeixeiraFortes1, Rossano Cesar Bonatto1, and Mario Ferreira Carpi1, 1Department of Pediatrics - Botucatu Medical School and 2Department of Microbiology and Immunology - Botucatu Bioscience Institute; Sao Paulo State University – UNESP

The IRF8-KLF4 Transcription Factor Cascade is Essential for the Development of Monocytes, Paper 154DaisukeKurotaki1,NaokiOsato1, AkiraNishiyama1, Michio Yamamoto1,TatsumaBan1, HideakiSato1,JunNakabayashi1, Marina Umehara1,MasatoshiNakazawa2,NorikoMiyake3,NaomichiMatsumoto3,KeikoOzato4,andTomohikoTamura1, 1Department of Immunology, 2Department of Experimental Animal Science, and 3Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan; 4Program in Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health,Bethesda,Maryland, United States of America

IRF8 and IRF1: Genomic Regulators of Innate Immunity, Paper 155DavidLanglais and Philippe Gros, Biochemistry Dept, Complex Traits Group, McGill University, Montreal, Canada

What Does Evolution Have to do with Inflammation?, Paper 156BrendaLaster, Department of Nuclear Engineering, Ben Gurion University, Beer Sheva 84105 Israel

Dynamin Inhibition Interferes with Cytokine Responses in Streptococcus Pyogenes-Infected Human Macrophages, Paper 157SinikkaLatvala1, Sanna Mäkelä1, Emmanuelle Charpentier2 and Ilkka Julkunen1 , 1Department of Infectious Disease Surveillance and Control, National Institute for Health and Welfare, Helsinki, Finland, 2Department of Molecular Biology, Umeå Centre for Medical Research, Sweden

Lymphopenia Modulates Levels of Signal Transducer and Activator of Transcription-1 Expression Leading to Enhanced CD4 T Cell Responsiveness to Type-I IFN, Paper 158CecileLeSaout1,RebeccaB.Hasley1,HiromiImamichi1,LuengTcheung1,MeganLuckey2,HyunPark2,ZonghuiHu3, Michael Sneller1,H.CliffordLane1 and Marta Catalfamo1 , 1CMRS/Laboratory of Immunoregulation, NIAID, NIH, Bethesda, MD, USA, 2Experimental Immunology Branch, CCR. NCI, NIH, Bethesda, MD, USA, 3Biostatistics Research Branch, DCR, NIAID, NIH, Bethesda, MD, USA



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Wound Healing Effects and Possible Mechanism of Action of the Butanol Fraction from Hydnocarpi Semen Crude Extract in Vitro Acute Inflammation Model, Paper 159GeumSeonLee1,3,KiManLee1,3,HongShim1,3,SeungHyunKim1,3,DongSoolYim1,JaeHoonCheong1,2 andTaeJinKang1,3*, 1College of Pharmacy, Sahmyook University, Seoul, 139-742 Korea 2Uimyung Research Institute for Neuroscience, Sahmyook University, Seoul, 139-742 Korea 3Institute of Chronic Disease, Sahmyook University, Seoul, 139-742 Korea

Aryl Hydrocarbon Receptor Negatively Regulates Type I Interferon Signaling in the Development of Murine Lupus, Paper 160SoyoungLee,BarryRipley,DavidMillrine,IchinoChinen,andTadamitsuKishimoto,Immune Regulation Laboratory, Osaka University World Premier International Immunology Frontier Research Center, Osaka, Japan

IL6 Promotes the Progression of Experimental Autoimmune Myocarditis to Dilated Cardiomyopathy, Paper 161JillianA.Legault1, G. Christian Baldeviano1, SuFey Ong 1,LeiWu1, Jobert G. Barin1,2,MonicaV.Talor1,DanielaCihakova1andNoelR. Rose1,2, 1Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 2Johns Hopkins School of Medicine, Baltimore, MD

Regulatory T Cells Modulate Systemic Illness Following Acute Lung Injury, Paper 162EfratLelkes,1, 2MarkR.Looney,3andMatthewF.Krummel2 , 1Department of Pediatrics, 3Department of Medicine, 2Department of Pathology, University of California, San Francisco, San Francisco, California, USA

Recombinant IL-37 Inhibits LPS Induced Inflammation in a SIGIRR- and MAPK-Dependent Manner, Paper 163SuzhaoLi1,Jaewoo,Hong2,MarcelF.Nold3,ClaudiaANold-Petry3,TaniaAzam1, Cecilia Garlanda4, Philip Bufler5,Soo-HyunKim2, Alberto Mantovani4,andCharles,A.Dinarello1, 1Department of Medicine, University of Colorado Denver, Aurora, Colorado USA, 2Institute of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea, 3Monash Institute of Medical Research, Monash University, Melbourne, Australia 4Research Institute Humanitas, Milan, Italy, 5Children’s Hospital, Ludwig-Maximilians University, Munich, Germany

The Serine Protease Plasmin Induces Expression of the CC-Chemokine Ligand 20 in Human Monocyte-Derived Dendritic Cells, Paper 164XuehuaLi,TatianaSyrovetsandThomasSimmet,Institute of Pharmacology of Natural Products & Clinical Pharmacology, Ulm University, Ulm, Germany

Critical Regulation of Type 2 Innate Lymphoid Cells by Mast Cells during Allergic Airway Inflammation, Paper 165HoyongLim1,YoungUkKim1,2and Yeonseok Chung1,2, 1)Center for Immunology and Autoimmune Diseases, Institute of Molecular Medicine, the University of Texas Medical School at Houston, Houston, Texas, USA, 2Graduate School of Biomedical Sciences, the University of Texas Health Science Center, Houston, Texas, USA

IL-7tv, a Modified Interleukin-7 Protein, is a Potent Agent for Immune Reconstitution, Paper 166AratiLimaye1, Ashley Iketani1, Rebecca Boohaker1, Jeremiah Oyer1,KathleenNemec1, Melhem Solh2,AlicjaCopik1, and Annette R. Khaled1, 1Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL USA. 2Florida Hospital Cancer Institute, Orlando, FL USA

Investigating the Mechanism of TLR Signaling Crosstalk in Mouse Macrophages, Paper 167BinLinandIainD.C.Fraser,Signaling Systems Unit, Laboratory of Systems Biology, NIAID, National Institutes of Health, Bethesda, Maryland, USA

IFN-Gamma Causes Aplastic Anemia by Altering HSC Composition and Interrupting Lineage Differentiation, Paper 168FanchingLin1, Bahara Saleh1,DeborahL.Hodge1,KimberlyBoelte1,TimChan1,JonathonP.Keller2andHowardA.Young1, 1Laboratory of Experimental Immunology, Cancer and Inflammation Program, 2Hematopoiesis and Stem Cell Biology Section, National Cancer Institute, Frederick, MD, USA

Direct in vitro Generation of Antigen Specific, Memory Phenotype, Cd8+ T Cells Using a Cocktailof Small Molecules and Gamma-Chain Cytokines, Paper 169AdamJ.Litterman,1DavidM.Zellmer,1 andDavidA.Largaespada1,2, Departments of 1Pediatrics and 2Genetics, Cell Biology and Development, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA



Targeting RIG-I-Like Receptor Signaling and Innate Immunity for Adjuvant Activity, Paper 170Yueh-MingLoo1,RanDong1, Courtney Wilkins1, Ernesto J. Munoz4, Sowmya Pattabhi2, Myra Wang4, John Grigg4,KristinM.Bedard4,KerryFowler4, Renee C. Ireton1, Shawn P. Iadonato4 and Michael Gale Jr. 1, 2, 3, Departments of 1Immunology, 2Pathology and 3Microbiology, University of Washington and 4KINETA, Inc., Seattle, WA, USA

IL-37 Suppresses Contact Hypersensitivity by Inducing Tolerogenic Dendritic Cells, Paper 171YuchunLuo1, Xiangna Cai1,SucaiLiu1, Sen Wang1,ClaudiaANold-Petry2,MarcelFNold2, Philip Bufler3,DavidANorris1, CharlesADinarello4 and MayumiFujita1 , Department of 1Dermatology and 4Medicine, University of Colorado School of Medicine, Aurora, CO, USA, 2The Ritchie Centre, Monash Institute of Medical Research, Monash University, Melbourne,Victoria, Australia, 3Children’s Hospital, Ludwig-Maximilians University, Munich, GermanyCrosstalk Between TLR4- and NOD2-Mediated Signaling in Inflammatory Bowel Disease: A Novel “Gain of Function” of the Crohn’s Disease-Associated 1007fs Mutation, Paper 172XiaojingMa1,2andHajeongKim1, 1SchoolofLifeSciences,ShanghaiJiaoTongUniversity,Shanghai,China,2DepartmentofMicrobiologyandImmunology,WeillCornellMedicalCollege,NewYork,USA

DominantRoleofIFN-λinRotavirusandReovirusDefenseExplainedbyPoorIFNAR1ExpressioninGutEpithelium, Paper 173TanelMahlakõiv1,2,3, PedroHernandez2,4 and Peter Staeheli1,2, 1Department of Virology, 2Institute of Medical Microbiology and Hygiene (IMMH), University of Freiburg Medical Center, Albert Ludwigs University Freiburg, 79104 Freiburg, Germany, 3Spemann Graduate School of Biology and Medicine (SGBM), Albert Ludwigs University Freiburg, 79104 Freiburg, Germany, 4International Max Planck Research School for Molecular and Cell Biology (IMPRS-MCB)

Induction of Antigen-Specific Regulatory T Cells as a Therapy for Autoimmune Diseases, Paper 174Anna M. Malara,ConorM.Finlay,AnnaM.Stefanska,KingstonH.G.Mills,School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland

The Role of Interferon Epsilon in the Immune Response in the Female Reproductive Tract, Paper 175NiamhE.Mangan1*,NollaigBourke1, KaYeeFung1, Sebastian Stifter1, Caroline Gargett2andPaulJ.Hertzog1, 1Centre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Victoria, Australia, 2Ritchie Centre, Monash Institute of Medical Research, Monash University, Victoria, Australia

Arid5a Contributes to Stabilization of IL-6 mRNA, and Elevation of IL-6 Level in vivo, Paper 176KazuyaMasuda1, Barry Ripley1,RikoNishimura2,TakashiMino3,OsamuTakeuchi3, Go Shioi4,HiroshiKiyonari4,andTadamitsuKishimoto1, 1Laboratory of Immune Regulation, World Premier International Immunology Frontier Research Center, and 2Departments of Molecular and Cellular Biochemistry, Graduate School of Dentistry, Osaka University, Osaka, Japan, 3Laboratory of Infection and Prevention, Institute for Virus Research, Kyoto University, Kyoto, Japan, and 4Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, Kobe, Japan

Maintenance of Memory Regulatory T Cells in Peripheral Tissues, Paper 177Megan M. Maurano,MichaelD.Rosenblum,Hong-AnTruong,AbulK.AbbasandIrisK.Gratz,University of California, San Francisco, USA

Characterization of PD-1+Tim-3+ ‘Exhausted’ CD8 T Cells in Mouse Models of Systemic Lupus Erythematosus, Paper 178TomMcCaughtry,IsharatYusuf,SandraGallagher,RonaldHerbst,LauraCarterandYueWangRespiratory, Inflammation & Autoimmunity, MedImmune LLC., Gaithersburg, MD

MIRNA Analysis Reveals Novel Insights into IL10 Function, Paper 179Claire E. McCoy1,2, Susan Quinn2, Michael P. Gantier1,KirstenFairfax3,LukeA.O’Neill2 and Bryan R.G. Williams1, 1Monash Institute of Medical Research, Monash University, Clayton, VIC, Australia, 2School of Biochemistry and Immunology, Trinity College Dublin, Ireland, 3Department of Immunology, Alfred Hospital, Monash University, VIC, Australia



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The TNF Family Member TL1A: A Key Player in Type 2 Immunity in Both Adaptive and Innate Lymphocytes, Paper 180FrançoiseMeylan1,EricHawley1,LukeBarron2, Jillian Barlow3,CuyianTan4 Pallavi Penumetcha1, Arianne Richard1, Xi Chen3, William E. Paul3 ThomasA.Wynn2, Igal Gery4,AndrewMcKenzie5 and Richard M. Siegel1 ,1Immunoregulation Section, Autoimmunity Branch, NIAMS. 2Immunopathogenesis Section, LPD, NIAID, 4Experimental Immunology Section, NEI, National Institutes of Health, Bethesda, MD USA, 5Laboratory of Molecular Biology Cambridge University, Cambridge , United Kingdom

PESTKA STUDENT AWARDRibavirin Enhances and Prolongs IFN Signaling and ISG Expression in Virally-Infected Human Lung Epithelial Cells, Paper 181A.N.MorrowandK.C.Zoon,National Institute of Allergy and Infectious Diseases, Bethesda, MD, USAIdentificationandCharacterizationofInterferon-λ4(IFN-λ4),ANovelClass-2CytokinewhichImpairsClearanceofHepatitisCVirus, Paper 182Brian Muchmore1,WeiTang1, Patricia Porter-Gill1,InduKohaar1,LuyangLiu1,NathanBrand1,HeiyoungPark2,HaroldDickensheets3, Faruk Sheikh3, Barbara Rehermann2,RaymondPDonnelly3,ThomasRO’Brien4 and LudmilaProkunina-Olsson1, 1Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA, 2Immunology Section, Liver Diseases Branch, National Institute for Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA, 3Division of Therapeutic Proteins, Center for Drug Evaluation & Research, US Food and Drug Administration, Bethesda, Maryland, USA, 4Infections and Immuno-epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA

Interferon Regulatory Factor-1 Protects Mice from Lethal Neuropathogenesis by Type-I IFN- Independent Local Antiviral Effects, Paper 183SharmilaNair,KatjaFinsterbusch,HansjörgHauser,AndreaKröger,Research Group of Innate Immunity and Infection, Helmholtz Centre for Infection Research, Braunschweig, Germany

DUSP11 is a Critical Regulator of Innate Immune Responses Mediated by Dendritic Cells, Paper 184KalyanC.Nallaparaju1,2, Yongliang Zhang1,XikuiLiu1, Joseph M. Reynolds1,RozaI.Nurieva1,2,andChenDong1,2, 1Department of Immunology, MD Anderson Cancer Center, Houston, TX, USA, 2The University of Texas Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, TX, USA

Cytokine Production in the Liver Modulate Hepatic Metabolism during Cachexia Progression, Paper 185RodrigoXNeves1,DanielaMRRiccardi1,MiguelLBatistaJr2,FabioLSantos1, Alex S Yamashita1, José C Rosa1 and Marília Seelaender1, 1Cancer Metabolism Research Group, Department of Cell and Developmental Biology, Institute of Biomedical Sciences,University of Sao Paulo, São Paulo, Brazil. 2Interdisciplinary Centre of Biochemistry, UMC, São Paulo, Brazil

Role of GTP-Mediated Structural Changes of MxA on its Antiviral Function against Influenza A, Paper 186PatriciaE.Nigg,DominikMüllerandJovanPavlovic,Institute of Medical Virology, University of Zurich, Zurich, Switzerland

Interleukin 37 Employs the IL-1 Family Inhibitory Receptor SIGIRR and the Alpha Chain of the IL-18 Receptor to Suppress Innate Immunity, Paper 187MarcelFNold1,2,ClaudiaANold-Petry1,2,CamdenLo3,SuzhaoLi2, Ina Rudloff1, Jarod A Zepp2,TaniaAzam2, Philip Bufler4, Cecilia Garlanda5, Alberto Mantovani5andCharlesADinarello2, 1The Ritchie Centre, Monash Institute of Medical Research,Melbourne, Victoria, Australia, 2Department of Medicine, University of Colorado,Denver, USA; 3Monash Micro Imaging, Monash University, Melbourne, Victoria, Australia; 4Children’s Hospital, Ludwig-Maximilians University, Munich, Germany; 5Istituto Clinico Humanitas, Milan, Italy

Dengue Infection Generates an Early NADPH-Oxidase Dependent ROS Production Required for Antiviral and Inflammatory Responses, Paper 188DavidOlagnier,CarmenNichols,ZhongHeandJohnHiscott,Vaccine & Gene Therapy Institute of Florida, Port Saint Lucie, Florida, USA



Differences in Cytokine Responses during Infection with High and Low Pathogenic Ebola Viruses, Paper 189JudithOlejnik 1, 2, Andrea Marzi 3,HeinzFeldmann 3 and Elke Mühlberger 1, 2, 1Department of Microbiology, 2National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, United States, 3Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States

Group-2 Innate Lymphoid Cell/ T cell Interactions in Helminth Expulsion, Paper 190Christopher J. Oliphant1,SeeHengWong1,5, Jennifer A. Walker1,YouYiHwang1,JillianL.Barlow1,EmilyHams4, Padraic G. Fallon2,3,4andAndrewN.J.McKenzie1, 1MRC Laboratory of Molecular Biology, Cambridge, UK, 2Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland, 3National Children’s Research Centre, Dublin, Ireland, 4Institute of Molecular Medicine, Trinity College Dublin, Dublin 2, Ireland, 5Present address: MedImmune, Milstein Building, Cambridge, UK

Difference in the Activation of IFN Gene Expression in Response to Influenza A and B Virus Entry, Paper 191PamelaÖsterlund , Sanna Mäkelä , Veera Arilahti, and Ilkka Julkunen, Virology Unit, National Institute for Health and Welfare, Helsinki, Finland

The Functional Analysis of RIG-I-Inducible MicroRNA, Paper 192Ryota Ouda1,KojiOnomoto2,KiyohiroTakahasi1,HirokiKato1, Mitstoshi Yoneyama2 and TakashiFujita1 , 1Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, 2Medical Mycology Research Center, Chiba University

Type I Interferon Treatment Inhibits the Formation of RNA Virus Replication-Associated Membrane Structures, Paper 193DiedeOudshoorn1, Corrine Beugeling1,RonaldW.A.L.Limpens2, Jochem Pronk1, Jessica Ruinard1,EricJ.Snijder1, Montserrat Bárcena2andMarjoleinKikkert1, 1 Department of Medical Microbiology, Section Molecular Virology, Leiden University Medical Center, Leiden, The Netherlands, 2 Department of Molecular Cell Biology, Section Electron Microscopy, Leiden University Medical Center, Leiden, The Netherlands

IRF8 Regulates Autophagy and Activates Microglia to Exacerbate Neuroinflammation, Paper 194KeikoOzato1, Ryusuke Yoshimi1, Yuko Yoshida1, Monica Gupta1,HiroakiYoshii1, Jeeva Munasinghe2, Olga Maximova3,HuabaoXiong4,HongshengWang5andHerbertCMorse,III5, 1Program in Genomics of Differentiation, NICHD, 2 Laboratory of Molecular Imaging, NINDS, 3Laboratory of Infectious Diseases, 5Laboratory of Immunogenetics, NIAID, National Institutes of Health, Bethesda MD, USA,4 Immunology Institute, Mt Sinai School of Medicine, New York, NY, USA

Type I Interferon Signaling Distinguishes Commensal from Virulent Staphylococcus Aureus, Paper 195DaneParker, Grace Soong, Paul Planet and Alice Prince, Department of Pediatrics, Columbia University, New York NY, USA

Interleukin-7-Mediated NFAT Activation Sets the Threshold for T Cell Development, Paper 196AmiyaK.Patra1, Andris Avots1, René P. Zahedi2,ThomasSchüler3, Albert Sickmann2,4, Ursula Bommhardt3 and Edgar Serfling1 , 1Department of Molecular Pathology, Institute of Pathology, University of Würzburg, Josef Schneider-Str. 2, D-97080 Würzburg, Germany, 2Department of Bioanalytics, Leibniz-Institute for Analytical Sciences – ISAS, Otto-Hahn-Str. 6b, D-44227 Dortmund, Germany, 3Institute of Molecular and Clinical Immunology, Otto-von-Guericke University Magdeburg Leipziger-Str. 44, D-39120 Magdeburg, Germany, 4Medical Proteom-Center (MPC),Ruhr-University Bochum, D-44801 Bochum, Germany

The Tyrosine-Based Motif of UNCc93B1 Differentially Regulates the Activity of Human Endosomal Toll-Like Receptors, Paper 197KarinPelka1,LarisaLabzin1, Rainer Stahl1, Jana Zimmermann2,StefanHoenig2 andEickeLatz1,3,4, 1Institute of Innate Immunity, University Hospitals Bonn, Bonn, Germany, 2Biochemistry-Center, University Hospitals Cologne, Cologne, Germany, 3UMass Medical School, Department of Infectious Diseases and Immunology, Worcester, MA, USA, 4German Center for Neurodegenerative Diseases, Bonn, Germany

Interleukin-1 Drives Hematopoietic Stem Cell Differentiation and Myelopoiesis via a Pu.1-Dependent Molecular Program, Paper 198 Eric M. Pietras1, Sarah Fong1,DirkLöffler2,RanjaniLakshminarasimhan1,Jose-MarcTechner1,TimmSchroeder2, and Emmanuelle Passegué1, 1The Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, University of California San Francisco, California, USA, 2Department of Biosystems Science and Engineering, Swiss Federal Institute of Technology, Zurich, Switzerland



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Beta-glucan Inducible microRNAs Negatively Regulate Inflammatory Response, Paper 199AlinaPoltajainen1, Sampsa Matikainen1,TuulaNyman2,HarriAlenius1 and Ville Veckman1, 1Finnish Institute of Occupational Health,DepartmentofSystemsToxicology,2InstituteofBiotechnology,UniversityofHelsinki

Pharmacodynamics of Immunotherapy for Opsoclonus-Myoclonus Syndrome: Impact on Cytokines/Chemokines, Paper 200Michael R. Pranzatelli,1 ElizabethD.Tate,1NathanR.McGee,1 and Richard M. Ransohoff2, 1National Pediatric Myoclonus Center, Department of Neurology, SIU School of Medicine, Springfield, IL; 2The Lerner Research Institute, Mellen Center for MS Treatment and Research, Cleveland Clinic Foundation, Cleveland,OH, USA

Interleukin-11 is the Dominant IL-6 Family Cytokine during Gastrointestinal Tumourigenesis, Paper 201TracyPutoczki1,NickWilson2,KirstenEdwards2,BrentMcKenzie2, Florian Greten3 and Matthias Ernst1,1Walter and Eliza Hall Institute of Medical Research, Melbourne,Victoria, Australia ,2CSL Ltd., Melbourne, Victoria, Australia, 3Institute of Pathology, Ludwig-Maximilian-University, Munich, Germany

IL-6 Inhibited Starvation-Induced Autophagy through STAT3/Bcl2/Beclin1 Pathway, Paper 202BeibeiQin,JianqinHeandShipingDing, The National Education Base for Basic Medical Sciences, School of Medicine, Zhejiang University, Hangzhou, 310029, Zhejiang Province, China

IL10 Inhibits Induction of miR-155 by Suppressing Ets2 - A Possible Mechanism for the Anti-Inflammatory Effects of IL10, Paper 23Susan R. Quinn,ClaireE.McCoy,andLukeA.O’Neill,School of Biochemistry and Immunology, Trinity College Dublin, Ireland

Inducible Nitric Oxide Synthase is Upregulated by IL-23/ IL-17A Axis in Inflammatory Bowel Disease: A Study in Algerian Patients, Paper 204HayetRafa1,HouriaSaoula2, Mourad Belkhelfa1,OussamaMedjeber1, Imene Soufli1,RymaToumi1,YvandeLaunoit3, Olivier Moralès3,M’hamedNakmouche2,NadiraDelhem3, and ChafiaTouilBoukoffa1 1Team: Cytokines and NOSynthases, Laboratory of Cellular and Molecular Biology (LBCM), Faculty of Biological Science, USTHB, Algiers, Algeria, 2Department of Gastroenterology, MaillotHospital, Algiers, Algeri, 3Institut de Biologie de Lille, UMR 8161, CNRS, Institut Pasteur de Lille, Universite´ Lille-Nord de France, Lille, France

The Convergence of IL-1 and Type I IFN on Antiviral Gene Networks is Regulated by Distinct IRF Family Member Cross-Talk, Paper 205HilarioJ.Ramos,GabrieleBlahnik,CourtneyWilkins,AlbertC.Huang,SeanProll,AimeeMcMillan,MichaelKatze,andMichaelGale Jr., Departments of Immunology and Microbiology, University of Washington School of Medicine, Seattle, WA 98195

Transcriptional Signatures of Pathogenesis and Successful Type I Interferon and Ribavirin Therapy in a Rhesus Macaque Model of MERS-CoV Infection, Paper 206AngelaL.Rasmussen1,DarrylFalzarano2, Emmie de Wit2, Friederike Feldmann3, Atsushi Okumura1,DanaP.Scott4,DouglasBrining4,TrentBushmaker5, Cynthia Martellaro2, Arndt G. Benecke6, Vincent J. Munster5,HeinzFeldmann2, and Michael G. Katze1, 1Department of Microbiology, University of Washington, Seattle,WA, USA ;2Disease Modeling and Transmission and 5Virus Ecology Units, Laboratory of Virology; 3Office of Operations Management; and 4Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases,National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA; 6Universite Pierre et Marie Curie, Centre National de la Recherche Scientifique, UMR7224, Paris, France

IL-27 Signals to Both B and T Cells Support Germinal Center Function and the Development of GC-Driven Lupus, Paper 207NorhananiMohdRedzwan1,DiptiVijayan1, Cindy Ma1,StuartTangye1,2, Robert Brink1,2, Carola Vinuesa3, and Marcel Batten1,2, 1Immunology Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia, 2St. Vincent’s Clinical School, University of New South Wales, Sydney, New South Wales, Australia, 3Department of Pathogens and Immunity, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia



Understanding the Mechanisms of Interferon Induction by a Large DNA Virus and its Application to Vaccine Development, Paper 208AnaLuisaReis,FuquanZhang,LynnetteGoatley,CharlesC.Abrams,DavidChapman,ChristopherL.Netherton,Haru-H.TakamatsuandLindaK.Dixon.The Pirbright Institute Pirbright, Woking, Surrey, United Kingdom

Towards the Identification Novel Regulators for Th1 Differentiation by Computational Genetics, Paper 209 Min Ren1,PengLi1, Ming Zheng2, Gary Peltz2,WarrenJ.Leonard1, 1Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA, 2Department of Anesthesia, Stanford University School of Medicine, Stanford, California, USA

Characterization of Human Interferon Subtype and Interferon-Stimulated Gene Signatures, Paper 210LynnseyA.Renn,TerenceC.Theisen,PhilippaHillyerandRonaldL.Rabin,Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, MD, USA

Cytokine Synthesis Profile from Different Adipose Pads during the Progression of Cachexia, Paper 211DanielaMRRiccardi1,RodrigoXNeves1,FelipeSHenrique2,MiguelLBatistaJr2,FabioLSantos1, Alex S. Yamashita1, José C Rosa1, Marília Seelaender1, 1Cancer Metabolism Research Group, Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil. 2Interdisciplinary Centre of Biochemistry, UMC, São Paulo, Brazil

Innate Neutrophil Function is Regulated Locally through IL-6 Control of Prostaglandins, Paper 212Christopher M Rice1, Claire J Greenhill1, Gareth W Jones1, Maceler Aldrovandi1,VictoriaJHammond1,ValerieBO’Donnell1, NicholasTopley2,PhilipRTaylor1 and Simon A Jones1, 1Cardiff Institute of Infection and Immunity, The School of Medicine, Cardiff University, 2 Institute of Translation, Innovation, Methodology & Engagement, The School of Medicine, Cardiff University

High-throughput SiRNA Screen to Identify Novel Signaling Molecules in the IL-17RA Signaling Pathway, Paper 213Erika Rickel1, Mike Ollmann2, Elisa Swearingen2,PaulKassner2,JenniferE.Towne1, Alison Budelsky 1 and Antony Symons1, 1Amgen, Seattle, Washington, USA, 2Amgen, San Francisco, California, USA

Type-IInterferonControlsitsOwnProductioninImmuneHomeostasisbyInducingPPAR-γExpressionandanInhibitoryPPAR-γ/IRF7Complex, Paper 214Barry Ripley1,MinoruFujimoto2,HiroshiTakemori2,SoyoungLee1, YongmeiHan2,LingliYang2, TomoharuOhkawara2, Satoshi Serada2, Ichino Chinen1,KazuyaMasuda1,TaroKawai1,TetsujiNaka2 andTadamitsuKishimoto1, 1Laboratory of Immune Regulation, Osaka University World Premier International Immunology Frontier Research Center, Osaka, Japan, 2 Laboratory for Immune Signal, National Institute of Biomedical Innovation, Osaka, Japan

Alternative Splicing Variants of Stimulator of Interferon Genes Present a Differential Ability to Induce Interferon Beta, Paper 215Estefanía Rodríguez-García,EstanislaoNistal-Villán,RobertoFerrero-LabordaandGloriaGonzález-Aseguinolaza,Division of Hepatology and Gene Therapy, Center for Applied Medical Research (CIMA), Pamplona, Spain

The Pro-Inflammatory Activities of Interleukin-6 are Mediated by the soluble Interleukin-6 Receptor via Trans-Signaling, Paper 216Stefan Rose-John, Department Biochemistry, University of Kiel, Kiel, Germany

BACH2 Represses Effector Differentiation and Cytokine Expression to Stabilize Treg-Mediated Immune Homeostasis, Paper 217R. Roychoudhuri1,K.Hirahara2,K.Mousavi2,D.Clever1, M. Bonelli2, G. Sciume2,H.Zare2, G. Vahedi2,C.Klebanoff1, V. Sartorelli2,Y.Kanno2,L.Gattinoni1,A.Nakamura3, A. Muto3, J. O’Shea2 andN.Restifo1, 1National Cancer Institute, National Institutes of Health, 2National Institute of Arthritis ,Musculoskeletal and Skin Diseases, Bethesda, MD, USA, 3Tohoku University, Sendai, Japan

Mechanisms of Lytic HSV-1 Clearance during Primary Infection of the Trigeminal Ganglia,Paper 218 DerekJ.Royer1,ChristopherD.Conrady1,DanielJ.J.Carr1,2, Departments of 1Microbiology and Immunology, and 2Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK USA



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STAT3 Induces Proapoptotic Signals in Chronic Lymphocytic Leukemia (CLL) Cells, Paper 219Uri Rozovski,DavidHarris,PingLi,ZhimingLiu,WuJiYuan,MichaelKeatingandZeevEstrov,Department of Leukemia, MD Anderson Cancer Center, Houston TX

Fibrinogen/CR3 Signaling Induces Demyelination by Promoting Th1 Cell Differentiation and Peripheral Macrophage Recruitment into the CNS, Paper 220JaeKyuRyu(1),KimM.Baeten(1), Mark A. Petersen(1,2), Sara G. Murray(1), Anke Meyer-Franke(1),DimitriosDavalos(1), Catherine Bedard(1),ThomasProd’homme(3), Israel F. Charo(1),HansLassmann(4),JayL.Degen(5), Scott S. Zamvil(3)andKaterinaAkassoglou(1,3)(1)Gladstone Inst., Univ. of California, San Francisco, San Francisco, CA, (2)Department of Pediatrics, Univ. of California, San Francisco, San Francisco, CA, (3)Department of Neurology, Univ. of California, San Francisco, San Francisco, CA, (4)Centre for Brain Research, Medical University of Vienna, Vienna, Austria, (5)Pediatrics, Univ. of Cincinnati, Cincinnati, OH

Post-Transcriptional Regulation of Interferon Gamma in Memory CD8+ T Cells, Paper 221Fiamma Salerno(1), Sander Engels(1),WanqiZhao(1),DeborahHodge(2),HowardA.Young(2), Jan Paul Medema(3), Monika C. Wolkers(1), (1)Department of Hematopoiesis, Sanquin Research, Amsterdam, The Netherlands; (2)Laboratory for Experimental Immunology, Cancer and Inflammation Program, Center of Cancer Research, National Cancer Institute at Frederick, USA; (3)

Laboratory of Experimental Oncology and Radiobiology (LEXOR), Center for Experimental Molecular Medicine (CEMM), Academic Medical Center (AMC), Amsterdam, The Netherlands

Cytokine Changes in Coinfected Subjects with Plasmodium and Intestinal Parasites in Naturally Exposed Populations to Malaria, Paper 222JuanC.Sánchez-Arcila(1),MarcelleMarcolinodeFrança(1),DaianadeSouzaPercedaSilva(2),RodrigoNunesRodriguesdaSilva(3), CesarinoJ.LimaAprígio(4), Mariana Pinheiro Alves Vasconcelos(5),DalmaM.Banic(2),JosuédaCostaLimaJúnior(1), Joseli de Oliveira Ferreira(1) (1) Laboratório de Imunoparasitologia, Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Rio de Janeiro, Brazil, (2)

Laboratório de Simulídeos e Oncocercose , Instituto Oswaldo Cruz/Fiocruz, Rio de Janeiro, Rio de Janeiro, Brazil, (3)Departamento de processamento final, Biomanguinhos/Fiocruz, Rio de Janeiro, Rio de Janeiro, Brazil, (4) Laboratório de Quimioterapia/Fiocruz, Porto Velho, Rondônia, Brazil and Universidade Federal de Rondônia, Porto Velho, Rondônia, Brazil, (5) Instituto de Infectologia Emilio Ribas, São Paulo, São Paulo, Brazil

A Novel Type I Interferon Antagonist Has in vivo Efficacy in a Model of SIV Infection in Rhesus Macaques, Paper 223NetanyaG.Sandler1,RichardT.Zhu1,JacobD.Estes2, Eli Boritz1, Srinivas Rao1,JeffreyD.Lifson2,DoronLevin3, Gideon Schreiber3, JeromeA.Langer4,DanielC.Douek1 1Vaccine Research Center, NIAID, NIH, Bethesda, MD, USA; 2AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA; 3Department of Biological Chemistry, Weizmann Inst., Rehovot, Israel; 4Department. of Pharmacology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ, USA

Resistance to Respiratory Syncytial Virus Replication is STAT1 and STAT2 Dependent, but I Interferon Independent, Paper 224Marvin Sandoval1,TroyCline2,Jian–DaLin3),SergeiV.Kotenko3,RussellK.Durbin1 andJoanE.Durbin1, 1Department of Pathology, New York University School of Medicine, New York, New York, USA, 2Department of Infectious Disease, St. Jude’s Children’s Research Hospital, Memphis, Tennessee, USA, 3Department of Biochemistry, New Jersey Medical School, Newark, New Jersey, USA

Inosine-Mediated Modulation of RNA Sensing by Innate Immune Sensors, Paper 225SoroushT.Sarvestani, Michael P. Gantier and Bryan R.G. Williams, Monash Institute of Medical Research, Monash University, Victoria, Australia

The Transcription Factor IRF8 is Required for the Development of Basophils, Paper 226HarukaSasaki1,DaisukeKurotak1,HideakiSato1,HerbertC.MorseIII2,KeikoOzato3 andTomohikoTamura1 ,1Department of Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan and 2Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases and 3Program in Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America

7:30 – 9:00 pm SPECIAL NETWORKING RECEPTION FOR STUDENTS, Seacliff A&B POSTDOCS AND NEW (1ST YEAR) FACULTY (Tickets Required) Sponsored by eBioscience



Wednesday, October 2, 2013

8:30 – 10:30 am PLENARY SESSION III: Cytokine Fundamentals – Grand Ballroom A Signaling, Expression and Epigenetics Chairs: Robert Schreiber,WashingtonUniversity,St.Louis,MO,USA and Giorgio Trinchieri,NationalCancerInstitute,NIH,Bethesda,MD,USA

8:30 – 9:00 am Cancer Immunoediting: Basic Mechanisms and Therapeutic Implications, Paper S-20 Robert Schreiber

9:00 – 9:30 am Type I Interferons and Innate Immune Sensing of Cancer TomGajewski, UniversityofChicago,Chicago,IL,USA

9:30 – 10:00 am Cancer Inflammation and Microbiota GiorgioTrinchieri

10:00 – 10:30 am Loss of Cutaneous TSLP Dependent Immune Responses Skews the Balance of Inflammation from Tumor-Protective to Tumor Promoting, Paper S-21 Freddy Radtke, Swiss Institute for ExperimentalCancerResearch,Lausanne,Switzerland

10:30 – 11:00 am Coffee Break- visit with the exhibitors Pacific Concourse


SYMPOSIUM T7: Cytokines in Infections Grand Ballroom A Chairs: Alan Sher,NationalInstituteofAllergyand InfectiousDiseases,NIH,Bethesda,MD,USAand Jody Baron, University of California, San Francisco, CA, USA

11:00 – 11:30 am The Role of IL-27 in Coordinating Treg Cell Activity ChrisHunter,University of Pennsylvania, Philadelphia, PA USA

11:30am – 12:00N New STATs on Memory CD8 T Cell Development SusanKaech,YaleUniversity,NewHaven,CT,USA

12:00 – 12:30 pm Initiation of Th2 Immunity Akiko Iwasaki, Yale University,NewHaven,CT,USA

12:30 – 1:00 pm Age-Dependent Hepatic Lymphoid Organization Directs Immune Priming, Cytokine Production, and Successful Immunity to Hepatitis B Virus, Paper S-3 Jody Baron

11:00am – 1:00pm SYMPOSIUM T8: Cytokine and Interferon Gene Regulation Grand B/C and Signaling I Chairs: Howard Young,NationalCancerInstitute,NIH,Frederick,MD,USA and Brendan Jenkins, Monash University, Victoria, Australia

11:00 – 11:30 am Cross-Talk between the IL-6 Cytokine Family and Pathogen Recognition Receptors in Cancer Brendan Jenkins

11:30am–12:00N Novel Technologies to Target STAT3 Pathway, Paper S-22 HuaYu,CityofHope,Duarte,CaliforniaUSA

12:00 – 12:30 pm Progressive Recruitment of STAT5 and Establishment of Unique H3K4me3 Marks during Pregnancy Define Mammary-Specific Gene, Paper S-23 LotharHennighausen,NationalInstitutesofDiabetes,Digestive,andKidneyDiseases, NIH,Health,Bethesda,MD,USA


12:30 – 1:00 pm Cytokine Regulation of the Molecular Balance between T-Bet and Bcl-6 in Effector Cell Responses, Paper S-24 Amy Weinmann, University of Washington, Seattle, WA, USA


2:00 – 3:45 pm CONCURRENT MINISYMPOSIA (Selected Submitted Abstracts)

2:00 – 3:45 pm MINISYMPOSIUM 5 Grand Ballroom A Chairs: Kathryn Zoon,NationalInstituteofAllergyand InfectiousDisease,NIHBethesda,MD,USA and Nancy Reich, Stony BrookUniversity,StonyBrook,NY,USA

2:00 – 2:15 pm Type-I Interferon Controls its Own Production in Immune Homeostasis by InducingPPAR-γExpressionandanInhibitoryPPAR-γ/IRF7Complex, Paper 214 Barry Ripley, Osaka University, Osaka, Japan

2:15 – 2:30 pm MTOR-Signaling Pathway Plays a Role in Induction of Autophagy by Type I Interferons, Paper 228 KathrynZoon

2:30 – 2:45 pm Dynamic Nuclear Trafficking of STAT5 Regulated by an Unconventional Nuclear Localization Signal, Paper 239 NancyReich

2:45 – 3:00 pm Cooperative Activation of Innate Lymphoid Type 2 Cells (ILC2) by Epithelial Cytokines in Response to Chitin, Paper 265 StevenVanDyken,UniversityofCalifornia,SanFrancisco,CA,USA

3:00 – 3:15 pm TSLP Driven Expansion and Activation of Type 2 Innate Lymphoid Cells is Augmented by IL-25 and IL-33, Paper 269 Michael Comeau, Amgen Inc., Seattle, WA, USA

3:15 - 3:30 pm The Cytokines IL-21 and GM-CSF Have Opposing Regulatory Roles in the Apoptosis of Conventional Dendritic Cells, Paper 270 EdwinChi-KeungWan NationalHeart,Lung,andBloodInstitute,NIH,Bethesda,MD,USA

CHRISTINA FLEISHMANN AWARD3:30 – 3:45 pm Essential Role of the Phosphatase PP1 in the RIG-I and MDA5 Mediated Antiviral Interferon Response, Paper 280 MichaelaGack,HarvardMedicalSchool,Boston,MA,USA

2:00 – 3:45 pm MINISYMPOSIUM 6 Grand B/C Chairs: Andrew Larner, Virginia Commonwealth University, Richmond, VA, USA and Richard Siegel,NationalInstituteof Arthritis,Metabolic,andSkinDiseases,NIH,Bethesda,MD,USA

2:00 – 2:15 pm Stat1 Inhibits Mitochondrial Biogenesis, Paper 247 AndrewLarner

2:15 – 2:30 pm Inflammatory Disease and an Impaired type I Interferon Response Resulting from a de novo human NEMO Hypomorphic Mutation, Paper 278 EricHanson,NationalInstituteofArthritis,Metabolic,andSkinDiseases,NIH, Bethesda,MD,USA

ICIS OUTSTANDING SCHOLAR AWARD, 2nd Place2:30 – 2:45 pm Assembly of IFNAR1/IFNAR2 is Regulated by Ubiquitin Specific Protease 18, Paper 281 Stephan Wilmes, University of Osnabrück, Osnabrück ,Germany


Wednesday, October 2, continued

ICIS POSTDOCTORAL INVESTIGATOR AWARD, Co-1st Place2:45 – 3:00 pm TSLP-Elicited Basophil Responses Mediate the Pathogenesis of Eosinophilic Esophagitis, Paper 282 EliaTaitWojno,UniversityofPennsylvania,Philadelphia,PA,USA

ICIS OUTSTANDING SCHOLAR AWARD, 1st Place3:00 – 3:15 pm IL-17-Signaling in LGR5-Positive Stem Cells Promotes Colon Tumorigenesis,Paper 296 JarodZepp,ClevelandClinicFoundationandClevelandClinicLernerCollegeofMedicine of Case Western Reserve University, Cleveland, Ohio USA

MILSTEIN YOUNG INVESTIGATOR AWARD3:15 – 3:30 pm Expression Screens Identify a Viral Bias in Interferon Effector Specificity and a Requirement for cGAS in Antiviral Immunity, Paper 298 JohnSchoggins,UniversityofTexasSouthwesternMedicalCenter,Dallas,TX,USA

PESTKA GRADUATE AWARD3:30 – 3:45 pm Protein Tyrosine Phosphatase Non-Receptor Type 22 Potentiates Toll-Like Receptor-Driven, Type 1 Interferon-Dependent Immunity, Paper 299 YayaWang,UniversityofMinnesota,Minneapolis,MNUSA

3:45 – 4:15 pm Coffee Break – visit with the exhibitors

4:15 – 5:45 pm CONCURRENT SYMPOSIA

SYMPOSIUM T9. Pattern Recognition Grand Ballroom A Chairs: Marco Colonna,WashingtonUniversity,St.Louis,MO,USA and Akiko Iwasaki,YaleUniversity,NewHaven,CT,USA

4:15 – 4:45 pm IL34 in Myeloid Cell Development Marco Colonna

4:45 – 5:15 pm Regulation and Function of the Toll-Like Receptor Family Gregory Barton, University of California, Berkeley, CA, USA

5:15 – 5:45 pm C-Type Lectin Receptors (CLRs), Pattern Recognition Receptors for Sensing Fungal Infection and their Signaling, Paper S-25 XinLin,MDAndersonCancerCenter,Houston,TX,USA

4:15 – 5:45 pm SYMPOSIUM T10: Cytokine and Interferon Gene Regulation Grand B/C and Signaling II Chairs: Sarah Gaffen, University of Pittsburgh, Pittsburgh, PA, USA and John Hiscott,VGTI-Florida,PortSt.Lucie,FL,USA

2013 MILSTEIN AWARD 4:15 – 4:45 pm IL-17 Signaling in Autoimmunity and Cancer XiaoxiaLi,ClevelandClinicFoundation,Cleveland,OH,USA

4:45 – 5:15 pm New Regulators of NF-κB-Dependent Inflammation SankarGhosh,ColumbiaUniversity,NewYork,NYUSA

5:15 – 5:45 pm Ubiquitination and Innate Immunity Averil Ma, University of California, San Francisco, CA USA

8:00 – 12:00 M CYTOKINES 2013 BANQUET Grand Ballroom A Followed By Entertainment

6:00 – 7:30 pm POSTER SESSION III (with wine and cheese) Pacific Concourse Papers: 227-270, 272-335



IL-27 Affects Helper T Cell Response via Regulation of PGE2 Production by Macrophages, Paper 227Yayoi Sato1,2,3,HiromitsuHara1, Shinobu Suzuki2,TsuneyasuKaisho3 and HirokiYoshida1 , 1Division of Molecular and Cellular Immunoscience, Department of Biomolecular Sciences, Faculty of Medicine, Saga University, 2 Dept. of Molecular & Cellular Biology, Kobe Pharma Research Institute, Nippon, Boehringer Ingelheim Co., Ltd.,3Laboratory of Immune Regulation, Immunology Frontier Research Center, Osaka University, Japan

MTOR-Signaling Pathway Plays a Role in Induction of Autophagy by Type I Interferons, Paper 228HanaSchmeisser1, Samuel B. Fey1,JulieHorowitz1, Elizabeth R. Fischer2, Corey A. Balinsky1,KotaroMiyake1, Joseph Bekisz1,AndrewL.Snow3 and KathrynC.Zoon1, 1National Institutes of Health, National Institute of Allergy and Infectious Disease, Cytokine Biology Section, Bethesda, MD, USA, 2National Institutes of Health, National Institute of Allergy and Infectious Disease, Rocky Mountain Laboratories, Research Technologies Section, Hamilton, MT, USA, 3Uniformed Services University of the Health Sciences, Department of Pharmacology, Bethesda, MD, USA

Dengue Virus Infection and Induction of Proinflammatory Cytokines in Dendritic Cells is Profoundly Inhibited by Selective Carbohydrate-Binding Agents (CBAs), Paper 229DominiqueSchols,MarijkeAlen,DanaHuskensandJanBalzarini,Rega Institute for Medical Research, Department of Microbiology and Immunology, University of Leuven, BE-3000 Leuven, Belgium

Unraveling the Role of Adam17 in IL-6 Trans-Signaling, Paper 230Jeanette Schwarz1, Isabell Yan2, Olga Will3, Paul Saftig1, Stefan-Rose-John1,Hans-WilliMittrücker2 and Athena Chalaris1, 1Institute for Biochemistry, CAU, Kiel, Germany, 2 Section Biomedical Imaging, UKSH, Kiel, Germany,3 Institute for Immunology, UKE, Hamburg, Germany

Type I Interferon Controls Gammaherpesvirus Latency, Paper 231Johannes Schwerk1,KendraBussey2,StefanLienenklaus3, Siegfried Weiss3, Melanie Brinkmann2,HansjörgHauser1 and MarioKöster1, 1DepartmentofGeneRegulationandDifferentiation,2Research Group of Viral Immune Modulation, 3DepartmentofMolecularImmunology,HelmholtzCentreforInfectionResearch,Braunschweig,Germany

Inhibition of IFN-Mediated STAT1 Activation in Intestinal Epithelial Cells by NSP1 - the Rotavirus-Encoded Inhibitor of IFN Induction, Paper 232Adrish Sen1, 2, 3andHarryGreenberg1, 2, 3, 1Dept of Microbiology & Immunology, 2Medicine, Stanford University, Stanford, California 94305. 3Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304

Multiparametric High Dimensional Analysis of Normal & VZV Infected Human Tonsil T Cells at a Single Cell Resolution by Mass Cytometry, Paper 234NandiniSen1,2,GourabMukherjee3, Sean C. Bendall2, Adrish Sen2,4, Astraea Jager2, Phil Sung1,GarryP.Nolan2, Iain Johnstone3, Ann M. Arvin1,2, 1Dept. of Pediatrics, 2Dept. of Microbiology & Immunolgy, 3Dept. of Statistics, 4Dept. of Gastroenterology, Stanford University, CA 94305, USA

Selective Regulation of CXCL1 Expression and Neutrophil Responses by Transcription Repressor Hes1, Paper 234Yingli Shang1,KarmenAu 1,XiaoyuHu 1,2 ,1Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, New York USA,2Department of Medicine, Weill Cornell Medical College, New York, New York USA

Effects of Dietary Fructo-Oligosaccharides on Gender- Based Differences in Gut Mucosal Cytokines, Paper 235PadmajaShastri1, Justin McCarville1, Stephen P.J. Brooks2,MartinKalmokoff3 and Julia M. Green-Johnson1, 1Applied Bioscience Graduate Program and Faculty of Science, University of Ontario Institute of Technology, Oshawa, Ontario , Canada L1H 7K4, 2 Bureau of Nutritional Sciences, Health Canada, Ottawa, Ontario, Canada K1A 0K9, 3 Atlantic Food and Horticulture Research Center, Agriculture and Agri-Food Canada, Kentville, Nova Scotia, Canada B4N 1J5

Computational Model for Mechanistic Investigation of Negative Feedback in Interleukin-17 Receptor Signaling, Paper 236Robert P. Sheehan,1 Abhishek Garg,2SarahL.Gaffen,2 and James R. Faeder1, 1Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA, 2Department of Medicine, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA



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Human BDCA2+BDCA3int Dendritic Cells are a Novel Functional Subtype of Classical Plasmacytoid Dendritic Cell, Paper 237TiffanyShih2,JihongDai1 and Patricia Fitzgerald-Bocarsly1,2, 1Department of Pathology and Laboratory Medicine, University of Medicine and Dentistry New Jersey-New Jersey Medical School, 2University of Medicine and Dentistry New Jersey-Graduate School of Biomedical Sciences, Newark, New Jersey, USA (UMDNJ-NJMS and GSBS will be transfer-red to Rutgers University, effective July 1, 2013

Homeostatic IL23R Signaling Limits Th17 Responses through IL22-Mediated Containment of Commensal Microbiota, Paper 238Vincent Feng-Sheng Shih1, Jennifer Cox1,4,NoelynKljavin2,HartRardin1, Michael Reichelt3,LindaRangell3,LauriDiehl3, WenjunOuyang1andNicoGhilardi1, 1Department of Immunology, 2Department of Molecular Biology, 3Department of Pathology, 4Present address: Novo Nordisk Research Center, 530 Fairview Ave N, Seattle WA, 98109

Dynamic Nuclear Trafficking of STAT5 Regulated by an Unconventional Nuclear Localization Signal, Paper 239HaYounShinandNancyC.Reich, Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York 11794

Characterization of Leukocyte Glucocorticoid Receptor Translocation in Response to Physical Stress, Paper 240Maria Y. Shiu1, Shawn G. Rhind2,AlexP.DiBattista1,RuthA.Lanius3,DonaldJ.Richardson3,4 and Rakesh Jetly5, 1Graduate Program, University of Toronto, Toronto, ON, Canada; 2Defence Research & Development (DRDC) Canada Toronto, Toronto, ON, Canada; 3Dept of Psychiatry, Schulich School of Medicine, Western University, London, ON, Canada; 4Parkwood Operational Stress Injury Clinic, St. Joseph’s Health Care, London, ON, Canada; 5Canadian Forces Health Services, Directorate of Mental Health, Dept of National Defence, Canada.

Increased IL-17C Production by the TLR3 Ligand Poly (I:C) in Primary Cystic Fibrosis Airway Epithelial Cells, Paper 241TsuyoshiShuto1,KeikoUeno-Shuto2,KouheiOnuki1,YukihiroTasaki1, Mary Ann Suico1andHirofumiKai1, 1Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan,2Laboratory of Pharmacology, Department of Pharmaceutical Sciences, Sojo University, Kumamoto, Japan

RNase L Induces Autophagy via C-Jun N-terminal Kinase and Double-Stranded RNA-Dependent Protein Kinase Signaling Pathway, Paper 242MohammadAdnanSiddiquiandKrishnamurthyMalathi, Department of Biological Sciences, University of Toledo, 2801 W. Bancroft St. Toledo, OH 43606

Evaluation of the Neonatal Cytokine Response: Basic Mechanisms of Activation via Toll-Like Receptors 2 and 4 in Monocytes from Term and Preterm Healthy Newborns, Paper 243AnaLucia Silveira-Lessa1, Camila Quinello2, Marco Antonio Cianciarullo2, Maria Esther J.R. Ceccon2, Magda Carneiro-Sampaio2, Patricia Palmeira2, 1Department of Parasitology, Institute of Biomedical Sciences, São Paulo, SP, Brazil, 2Department of Pediatrics, Medical School, University of São Paulo, São Paulo, SP, Brazil Homologous 2’,5’-Phosphodiesterasesf from Disparate RNA Viruses Antagonize Antiviral Innate Immunity, Paper 244RobertH.Silverman1, Rong Zhang2,BabalK.Jha1,KristenM.Ogden3,BeihuaDong1, Ruth Elliott2,LingZhao2,JohnT.Patton3, and Susan R. Weiss2 , 1Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA,2

Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA,USA, 3Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA

Antiviral and Cytokine Modulating Potential of Chlorophytum borivilianum Hot Aqueous Extract, Paper 245Balendra Singh1,SharadK.Yadav2, 1Department of Biotechnology, Bundelkhand University, Jhansi, 2Department of Microbiology & Immunology, College of Veterinary Science, DUVASU Mathura, India

TSLP-Mediated Extramedullary Hematopoiesis Promotes Allergic Inflammation, Paper 246Mark C. Siracusa1,EliaD.TaitWojno1,LisaC.Osborne1, Steven A. Saenz1,BrianS.Kim1, Alain J. Benitez3,KathrynR.Ruymann4,DonnaL.Farber5, Patrick M. Sleiman6-8,HakonHakonarson6-8, Antonella Cianferoni4,Mei-LunWang3, Jonathan M. Spergel4, Michael R. Comeau9,andDavidArtis1,2,1Department of Microbiology, Institute for Immunology, and 2Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; 3Division of Gastroenterology, Hepatology, and Nutrition, and 4Department of Pediatrics, Division of Allergy and Immunology, Children’s Hospital of Philadelphia, Philadelphia, PA 19104, USA; 5Department of Surgery and the Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY 10032, USA; 6Center for Applied Genomics and 7Division of Human Genetics, Abramson Research Center, The Children’s Hospital of Philadelphia, and 8Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; 9Inflammation Research, Amgen Inc., Seattle, WA 98119, USA


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Stat1 Inhibits Mitochondrial Biogenesis, Paper 247Jennifer Sisler1, Magdalena Szelag1,VidishaRaje1,MartaDerecka1 ,KarolSzczepanek1, 2,EdwardLesnefsky1,2 and Andrew C. Larner1,3 , 1 Department of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298,USA, 2Medical Service, McGuire Department of Veterans Affairs Medical Center, Richmond, VA 23249, USA

Insights into the Evolution of Class II Cytokines: Crystal Structure of Interleukin 22 from Zebrafish, Paper 248Piotr Siupka1,OleJ.Hamming1,Jean-PierreLevraud2,RuneHartmann1, 1Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark; 2Macrophages et Développement de l’Immunité, Institut Pasteur, Paris, France

The Role of Type I Interferons in Suppressing Breast Cancer Metastasis to Bone, Paper 249Clare Y. Slaney1, Jai Rautela1,2,3,BradleyN.Bidwell2,RobinL.Anderson2,3,4,PaulJ.Hertzog5 and Belinda S. Parker1, 1Department of Biochemistry, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia, 2Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia, 3Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia, 4Department of Pathology, University of Melbourne, Parkville, Victoria, Australia, 5Centre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia

Selective Regulation of Cytokine and Chemokine Expression by the Notch Pathway, Paper 250Sinead Smith1, Yingli Shang1,HaixiaXu1, Jimmy Zhu1, Baohong Zhao1, Chao Shi2,RyoichiroKageyama3,LionelB.Ivashkiv1,4, Xiaoyu Hu1,5, 1Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY, USA; 2Rockefeller University, New York, NY, USA, 3Kyoto University, Kyoto, Japan; 4Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY, USA; 5Department of Medicine, Weill Cornell Medical College, New York, NY, USA

The Role of Chemokine Receptor CCR7 and Its Ligands CCL19 and CCL21 in Tumor Progression of Pancreatic Ductal Adenocarcinoma, Paper 251Jan Sperveslage1, Sunna Frank2,CarolaHeneweer3, Jan Egberts4, Bodo Schniewind4, Malte Buchholz5,Frank Bergmann6,NathaliaGiese7, Johanna Munding8,StephanHahn9,HolgerKalthoff4,GuenterKloeppel2,10 and Bence Sipos1, 1Institute of Pathology, University of Tuebingen, Germany, 2Department of Pathology, University of Kiel, Germany, 3Department of Diagnostic Radiology, University of Kiel, Germany, 4Molecular Oncology Section,Department of General Surgery, University of Kiel, Germany,5Department of Gastroenterology, University Hospital, Philipps University, Marburg, Germany, 6Department of Pathology and 7Department of Surgery University of Heidelberg, Germany, 8Department of Pathology and 9Internal Medicine,Ruhr University, Bochum, Germany, 10Department of Pathology, Technical University of Muenchen, Germany

Analysis of a Cross-Talk between Various Chemokines and Bone Marrow-Derived Stem Cells in Patients with Pancreatic Cancer, Paper 252TeresaStarzyńska1, WojciechBlogowski1, Marta Budkowska2,DariaSałata2,KrzysztofDąbkowski1,andBarbaraDołęgowska2, 1Department of Gastroenterology and 2Department of Medical Analytics, Pomeranian Medical University in Szczecin, Poland

IL-36 Induces Inflammation and Collagen Deposition in the Lung, Paper 253Yu Sun1, Afsaneh Mozaffarian1,HeatherA.Arnett1,HuyenDinh1,EstherS.Trueblood2, and JenniferE.Towne1, 1Inflammation and 2Pathology, Amgen Inc, Seattle, WA USA

Association of Interferon Stimulated Genes and IRF9 Upregulation with Drug Resistance in Multicellular Spheroids and Monolayer Cells upon Crowding, Paper 254KatjaPokrovskajaTamm1,IrynaKolosenko1, Mårten Fryknäs2, Per Johnsson1, Sofi Forsberg1,SlavicaBrnjic1,HanifRassoolzadeh1, Paola Pellegrini1,DanGrandér1,RolfLarsson2,StigLinder1 andAngeloDeMilito1, 1Department of Oncology&Pathology, Karolinska Institutet, Stockholm, Sweden, 2Division of Clinical Pharmacology, Department of Medical Sciences, Uppsala University Hospital, 751 85 Uppsala, Sweden

Inhibition of Dectin-1 Signaling Suppresses Colitis by Regulating the Balance of Intestinal Microbiota and Cellular Immunity, Paper 255CeTang1, 2, 3,TomonoriKamiya4,MotohikoKadoki1, 2, and Yoichiro Iwakura1, 2, 3, 4, 1Research Institute for Biomedical Sciences, Tokyo University of Science, Noda-shi Chiba, Japan 2Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan, 3Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Saitama, Japan, 4Graduate School of Science, the University of Tokyo, Minato-ku, Tokyo, Japan

MAPPIT and Co: The Importance of System Artifacts, Paper 256JanTavernier,LeentjeDeCeuninck,SarahGerlo,IrmaLemmens,SamLievens,JoséVanderHeydenandJorisWauman,VIB Dept. Medical Protein Research, Ghent University, Belgium



Development of a Hyperglycosylated Interferon ALFACON1: Towards Monthly Dosing for Antiviral Therapies, in Diseases Such as Chronic Hepatitis C, Paper 257JoshuaS.Taylor1, Qingling Zhang1, Justin G. Julander2,AntitsaD.Stoycheva1,HuaTan1, Christabel V. Moy1, Sushmita Chanda1, Julian A. Symons1,LeoN.Beigelman1,LawrenceM.Blatt1,andJinHong1, 1Alios BioPharma, 260 E Grand Ave. 2nd Floor, South San Francisco, CA 94080, USA, 2Utah State University, 1400 Old Main Hill, Logan, UT 84322, USA

Bone-Targeting Properties of the IL-27/IL-30 Poly-Glutamic Acid Motif, Paper 258AurélieJeanneTormo1,LindaAnnBeaupré1, Greg Elson 2, Sandrine Crabé 1,3 and Jean-François Gauchat 1, 1 Département de Pharmacologie, Université de Montréal, Montreal QC, Canada. 2NovImmune SA, Geneva, Switzerland, 3Present address: Wittycell, Evry, France

Lipopolysaccharide Decreases SIGIRR/TIR8 Gene Expression by Suppressing Sp1 via TLR4-p38 Mapkinase Pathway in Monocytes and Neutrophils, Paper 259KeikoUeno-Shuto,1,*TsuyoshiShuto,2,*KosukeKato,2,3 Miki Sato,2 KeizoSato,4HiromichiSakai,2TomomiOno,2 Mary Ann Suico,2YujiUchida,1NaofumiTokutomi,1 andHirofumiKai2, 1 Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Global COE “Cell Fate Regulation Research and Education Unit”, Kumamoto University, Kumamoto, Japan, 2 Laboratory of Pharmacology, Division of Life Science, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto, Japan, 3 Department of Physiology & Lung Center, Temple University School of Medicine, Philadelphia, PA, USA, 4 School of Pharmacy, Kyushu University of Health and Welfare, Yoshino Nobeoka, Miyazaki, Japan

Association of Polymorphic Variation of MCP-1 (-2518 A/G) SNP with Clinical Symptomsin Systemic Lupus Erythematosus Patients from Western India, Paper 260Vinod Umare(1), Vandana Pradhan(1),AnjaliRajadhyaksha(2),KanjakshaGhosh(1)andAnitaNadkarni(1) , (1) National Institute of Imunohaematology, (Indian Council of Medical Research), Mumbai, Maharashtra, India, (2) Department of Medicine, King Edward Memorial Hospital, Mumbai, Maharashtra, India

Outcome of Naïve Actemra Therapy in Patients with Rheumatoid Arthritis Using Multi-Plex Analysis, Paper 261KazukoUno (1), Mitsuhiro Iwahashi (2),MikiTanigawa(3),KatsumiYagi(1) andKazuyukiYoshizaki(3), (1)Louis Pasteur Center for Medical Research, Kyoto, Japan, (2)Higashi Hiroshima Memorial Hospital, Hiroshima, Japan, (3)Osaka University, Osaka, Japan

Viperin vs. Tick-Borne Encephalitis Virus: Mechanisms of a Potent Antiviral Protein, Paper 262Arunkumar S. Upadhyay1,KirstinVonderstein1, Andreas Pichlmair2, Oliver Stehling3,Ju-TaoGuo4,RolandLill3, Friedemann Weber3 and AnnaK.Överby1 , 1Umeå University, Sweden; 2Max-Planck Institute of Biochemistry, Munich, Germany; 3Philipps-University Marburg, Germany; 4Drexel University College of Medicine, Doylestown, USA

IFN-Gamma Reprograms IFN-Beta-Induced Signaling Pathways in Human Monocytes , Paper 263AnetteH.H.VanBoxel-Dezaire and George R. Stark. Department of Molecular Genetics, Cleveland Clinic, Cleveland, Ohio, USA

Production and Extreme RNA Editing of Defective Interfering Particles is Associated with Interferon Induction by Human Metapneumovirus, Paper 264 BernadetteG.vandenHoogen,SandervanBoheemen,JonnekedeRijk,TheoBestebroer,AlbertD.M.E.Osterhaus,andRonA.M. Fouchier, Erasmus MC - Department of Viroscience, Rotterdam, The Netherlands

Cooperative Activation of Innate Lymphoid Type 2 Cells (ILC2) by Epithelial Cytokines in Response to Chitin, Paper 265StevenJ.VanDyken,AlexanderMohapatra,JesseC.Nussbaum,Hong-ErhLiang,andRichardM.Locksley,Departments of Medicine and Microbiology/Immunology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143

Host Restriction Factor SAMHD1 Limits Human Retrovirus Infection of Primary Monocytes via the Innate Sensor STING, Paper 266Julien VanGrevenynghe1, 2, Alexander Sze2, Mehdi Belgnaoui2,RongtuanLin2 and JohnHiscott1, 1VGTI-Florida, Port St. Lucie FL; 2Lady Davis Inst., Jewish General Hospital, McGill University, Montreal Canada

Challenging the Th1 Paradigm: A Detrimental Role for IFN-Gamma and IFN-Regulated CD64 in Human Leishmaniasis Paper 267Johan Van Weyenbergh1,3,TheoThepen4, George Soares1,RicardoKhouri1, Stefan Barth4,5, Gilvaneia Silva-Santos1, Jackson M Costa2, Aldina Barral2,3andManoelBarral-Netto1,3, 1LIMI, 2LIP, Gonçalo Moniz Research Center, Oswaldo Cruz Foundation (FIOCRUZ), Salvador-Bahia, 3Institute for Immunological Investigation, iii-INCT, São Paulo-SP, Brazil. 4Fraunhofer IME, Department of Pharmaceutical Product Development, 5Helmholtz-Institute for Biomedical Engineering,Department of Experimental Medicine and Immunotherapy, University Hospital RWTH Aachen, Germany



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Effect of Dystonia-Causing Point Mutation in PACT on Activation of Interferon-Induced Protein Kinase PKR, Paper 268LaurenSVaughn1,D.CristopherBragg2,NutanSharma2, Sarah Camargos3, Francisco Cardoso3, and Rekha C Patel1, 1University of South Carolina, Department of Biology, Columbia, SC, USA, 2Massachusetts General Hospital, Department of Neurology, Charlestown MA, USA, 3Federal University of Minas Gerais, Department of Internal Medicine, Belo Horizonte, MG, Brazil

TSLP Driven Expansion and Activation of Type 2 Innate Lymphoid Cells is Augmented by IL-25 and IL-33, Paper 269Christine Vissinga1,TodMartin1,HeidiK.Jessup2and Michael R. Comeau1 , 1Inflammation Research, Amgen Inc., Seattle, WA USA, 2Cellular Immunology, Novo Nordisk, Seattle, WA USA

The Cytokines IL-21 and GM-CSF Have Opposing Regulatory Roles in the Apoptosis of Conventional Dendritic Cells, Paper 270EdwinChi-KeungWan1, Jangsuk Oh1,PengLi1, Erin E. West1, Elizabeth A. Wong1, Allison B. Andraski1, Rosanne Spolski1, Zu-Xi Yu2,JianpingHe3,BrianL.Kelsall3, WarrenJ.Leonard1, 1Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1674, 2Pathology Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1674, 3Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1674

The Psoriasis-Associated D10N Variant of the Adaptor Act1 with Impaired Regulation by the Molecular Chaperone Hsp90, Paper 272Chenhui Wang1,10,LingWu1,2,10,KatarzynaBulek1,BradleyNMartin1,2, Jarod A Zepp1,ZizhenKang1,CainiLiu1,TomaszHerjan1, Saurav Misra3, Julie A Carman4, Ji Gao4,AshokDongre4,ShujieHan5,KevinDBunting5,JenniferSKo6,HuiXiao7,VijayKKuchroo8, WenjunOuyang9andXiaoxiaLi1, 1Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA, 2Department of Pathology, Case Western Reserve University, School of Medicine, Cleveland, Ohio,USA, 3Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA, 4Discovery Biology, Bristol-Myers Squibb, Princeton, New Jersey, USA, 5Aflac Cancer & Blood Disorders Center of Children’s Healthcare of Atlanta and Emory University Department of Pediatrics, Atlanta, Georgia, USA, 6Department of Anatomic Pathology & Clinical Pathology, Cleveland Clinic Foundation, Cleveland Ohio, USA, 7Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China,8Center forNeurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School,Boston, Massachusetts, USA, 9Department of Immunology, Genentech, South SanFrancisco, California, USA, 10These authors contributed equally to this work.

Antibody Deficiency Associated with an Inherited Autosomal Dominant Mutation in TWEAK. Paper 273Hong-YingWang1, Chi A. Ma1, Yongge Zhao1, Xiying Fan1,Qing Zhou2, Pamela Edmonds1, Gulbu Uzel3, Joao Bosco Oliveria4, Jordan Orange5 and Ashish Jain1, 1Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases (NIAID), 2Inflammatory Disease Section, National Human Genome Research, Institute, 3Immunopathogenesis Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, 4Department of Laboratory Medicine, Clinical Center, National Institutes of Health (NIH), Bethesda, MD 20892, 5Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104InvolvementofActivatingtheβ-Catenin-DependentPathwayandDecreasingIFN-GammaProductioninDexamethasone-Induced Tolerogenic Dendritic Cells, Paper 274Jia WangandYiLiu,Department of Rheumatology and Immunology, West China Hospital, Si Chuan University, Chengdu, Sichuan, China, 610041

The Transcription Factor IRF8 Overrides BCR-ABL to Rescue Dendritic Cell Development in Chronic Myeloid Leukemia, Paper 275TomoyaWatanabe1,2,ChieHotta1,Shin-ichiKoizumi1,KazuhoMiyashita1,3,JunNakabayashi1,DaisukeKurotaki1, Go R. Sato1, Michio Yamamoto1,AkiraNishiyama1, Michiko Aihara2, Yoshiaki Ishigatsubo3, and TomohikoTamura1, 1Department of Immunology, 2

Department of Environmental Immuno-Dermatology, and 3Department of Internal Medicine and Clinical Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Type I Interferon Protects Against Lethal Langat Virus Infection, Paper 276Elvira Weber1,KatjaFinsterbusch2,RichardLindquist1,AndreaKröger2,andAnnaÖverby1 , 1Department of Clincial Microbiology, University of Umeå, Umeå, Sweden, 2HZI, Braunschweig, Germany

Simultaneous Measurement of 13 Porcine Cytokines/Chemokines Using MILLIPLEX® MAP Technology, Paper 277TraciWenteandQiangXiao,EMD Millipore, Bioscience Division, St Charles, MO



Inflammatory disease and an Impaired Type I Interferon Response Resulting from a de novo Human NEMO Hypomorphic Mutation, Paper 278Alex W. Wessel1,AmyP.Hsu2, Jevgenia Zilberman-Rudenko1,RaphaelaT.Goldbach-Mansky3, Richard M. Siegel1, and Eric P. Hanson1 ,1Autoimmunity Branch, NIAMS, 2Laboratory of Clinical Infectious Diseases, 3NIAID, Pediatric Translational Research Branch, NIAMS, Bethesda, MD

Experimental Analysis of Acute Murine Oral Candidiasis after in vivo Anti-IL-17A / IL-17F Treatment and in Knockout Mice, Paper 279NatashaWhibley1, Anna J. Mamo1,ElisabettaTraggiai2,FrankKolbinger2, Beate Vogel2,MichaelKammüller2, Ulrich Siebenlist3 andSarahL.Gaffen1, 1 Division of Rheumatology and Clinical Immunology, University of Pittsburgh, 2 Novartis Institutes for Biomedical Research, Basel, Switzerland, 3 NIAID, NIH, Bethesda MD

Essential Role of the Phosphatase PP1 in the RIG-I and MDA5 Mediated Antiviral Interferon Response, Paper 280Effi Wies1,MayK.Wang1,2,NatalyaP.Maharaj1,KanChen1, Shenghua Zhou3, Robert W. Finberg3, and Michaela U. Gack1,2 , 1New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts, USA 2Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA ,3 Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA

Assembly of IFNAR1/IFNAR2 is Regulated by Ubiquitin Specific Protease 18, Paper 281Stephan Wilmes1,ZhiLi2,KatharinaHötte1, Oliver Beutel1,CindyKroll1, Friedrich Roder1,PatriziaHanhart1DennisJanning1, ChangjiangYou1, Christian Paolo Richter1,VéroniqueFrançois-Newton2, Gilles Uzé3, Sandra Pellegrini2 and Jacob Piehler1, 1University of Osnabrück, FB Biology, Department of Biophysics, Osnabrück, Germany, 2Institut Pasteur, Départment Immunologie, Unité de Signalisation de Cytokines, Paris, France, 3CNRS UMR 5235, University Montpellier II, Place Eugène Bataillon, 34095 Montpellier cedex 5, France

TSLP-Elicited Basophil Responses Mediate the Pathogenesis of Eosinophilic Esophagitis, Paper 282EliaD.TaitWojno1,2,21, MarioNoti1,2,21,BrianS.Kim1,2, Mark C. Siracusa1,2, Paul R. Giacomin1,2,4,MeeraG.Nair1,2, Alain J. Benitez5,KathrynR.Ruymann6, Amanda B. Muir5,DavidA.Hill1,2,KudakwasheR.Chikwava7, Amin E. Moghaddam8, Quentin J. Sattentau8, Aneesh Alex9-11, Chao Zhou9-11,PaulMenard-Katcher12,MasatoKubo13,14,KazushigeObata-Ninomiya15,16,HajimeKarasuyama15,16, Michael R. Comeau17,TerriBrown-Whitehorn6, Patrick M. Sleiman18-20,HakonHakonarson18-20, Antonella Cianferoni6, Gary W. Falk12,Mei-LunWang5, Jonathan M. Spergel6,andDavidArtis1,2,3, 1Department of Microbiology and 2Institute for Immunology, Perelman School of Medicine and 3Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA, 4Queensland Tropical Health Alliance and School of Public Health and Tropical Medicine, James Cook University, Cairns, Australia; 5Division of Gastroenterology, Hepatology, and Nutrition, Children’s Hospital of Philadelphia, Philadelphia, PA, USA, 6Department of Pediatrics, Division of Allergy and Immunology, Children’s Hospital of Philadelphia, Philadelphia, PA, USA;7Department of Pathology and Laboratory Medicine, Children’s Hospital of Philadelphia, Philadelphia, PA, USA, 8The Sir William Dunn School of Pathology, The University of Oxford, Oxford, UK; 9Department of Electrical and Computer Engineering, 10Center for Photonics and Nanoelectronics, and 11Bioengineering Program, Lehigh University, Bethlehem, PA, USA, 12Division of Gastroenterology, Hospital of the University of Pennsylvania, Philadelphia, PA, USA; 13Laboratory for Signal Network, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama and 14Division ofMolecular Pathology, Research Institute for Biological Science, Tokyo University of Science, Chiba, Japan, 15Department of Immune Regulation and 16JST, CREST, Tokyo Medical and Dental University Graduate School, Tokyo, Japan; 17Inflammation Research, Amgen Inc., Seattle, WA, USA, 18Center for Applied Genomics and 19Division of Human Genetics, Abramson Research Center, The Children’s Hospital of Philadelphia and 20Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA, 21These authors contributed equally to this work.

Suppression of SMAD-1 Signaling Pathway in Mouse Lung Tissue Remodelling by Oncostatin M, Paper 283StevenWong,RebeccaRodrigues,ChristineKerrandCarlD.Richards,McMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton,Ontario, Canada

Caspase-8-Independent Role of c-FLIP in Inflammasome Activation, Paper 284Yung-HsuanWu1,Wen-ChiKuo1, Yu-Jong Wu1,2,Kai-TingYang1,Shui-TeinChen3,Si-TseJiang4,andMing-ZongLai1,2, 1Institute of Molecular Biology and 3Institute of Biological Chemistry, Academia Sinica,Taipei, Taiwan, 2Institute of Immunology, National Taiwan University, Taipei,Taiwan, 4National Laboratory Animal Center, National Applied Research Laboratories, Tainan, Taiwan

International Cytokine and Interferon SocietyInternational Cytokine and Interferon Society


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Interferon Regulatory Factor 8 is Essential for Regulating the Response of Microglia to Neuronal Injury, Paper 285RuiDanXie1,NàdiaVillacampa2, Carsten Minten1,RachaelTerry3,NicholasJ.C.King3, Beatriz Almolda2,BertaGonzález2, Bernardo Castellano2,andIainL.Campbell1, 1 School of Molecular Bioscience & Bosch Institute, University of Sydney, Sydney, NSW Australia 2Medical Histology, Institut de Neurociències, Universitat Autònoma de Barcelona, Barcelona, Spain 3Discipline of Pathology & Bosch Institute, University of Sydney, Sydney, NSW Australia

Regulation of Autophagy by E3 Ubiquitin Ligase Triad3A through Beclin 1 Ubiquitination, Paper 286Congfeng Xu, Yi Zhang, and Yanyun Zhang, Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine (SJTUSM) and Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences & SJTUSM, Shanghai, China

Th17-Producing IL-17 on Periodontal Ligament Induced Root Resorption in Mouse Models of Rheumatoid Arthritis and Atopic Dermatitis, Paper 287Masaru Yamaguchi,KunihikoYamada,MamiShimizu,TomokazuYoshino,JunKikutaandKazutakaKasai,Department of Orthodontics, Nihon University School of Dentistry at Matsudo

Identification of an Anti-Viral Compound with Inhibitory Effects on Influenza Replication, Paper 288CindyL.H.Yang1,AnnaH.Y.Law2, TerryC.T.Or1,2,K.Y.Au2,JamesC.B.Li1,2,AllanS.Y.Lau1,2 ,1BioScreening Unit, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Specia Administrative Region, People’s Republic of China 2Cytokine Biology Group, Department of Paediatrics and Adolescent Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, People’s Republic of China

Triptolide Mediated-Inhibition of Interferon Signaling Enhances Vesicular Stomatitis Virus Based Oncolysis, Paper 289Fethia Ben Yebdri1, Julien VanGrevenynghe1,3,VeraATang2,Marie-LineGoulet1,JianHuiWu1,DavidFStojdl2, John Hiscott1,3 and RongtuanLin1 ,1Lady Davis Institute-Jewish General Hospital, McGill University, Montréal, Canada, 2Children’s Hospital of Eastern Ontario Research Institute, Ottawa, Canada, 3Division of Infectious Diseases, VGTI Florida, Port Saint Lucie, Florida, USA

The Protein Kinase R as a Repressor of Inflammasome Activity, Paper 290HowardC.H.Yim1, Agnieszka Pindel1, Arindam Chakrabarti2, Pieter Faber2, Robert Silverman2, Bryan R.G. Williams1,and Anthony J. Sadler1 , 1Centre for Cancer Research, Monash Institute of Medical Research, Monash University, Australia, 2Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, USA

Tumor Necrosis Factor –ΑAggravates Orthodontically Root Resorption, Paper 291T.Yoshino,M.Yamaguchi,K.Yamada,M.ShimizuandK.Kasai,Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Matsudo, Japan

TheRoleofIL-6withTNF-αorIL-1onInductionofInflammatoryAnemiathroughHepcidininDifferentChronicInflammatory Disease, Paper 292KazuyukiYoshizakiandSoken-NakazawaJ.Song,Department Immuno-Medical Science, Office for University-Industry Collaboration, Bld. Incubation A-407, Osaka University, 2-1 Yamadaoka,Suita, Osaka 565-0871, Japan

Anti-Inflammatory Effect of Kopetdaghins A, C and E from Dorema Kopetdaghense, Paper 293ShahrzadZamaniTaghizadehRabe 1, Mehrdad Iranshahi 2, Mahmoud Mahmoudi *1, Maryam Rastin 1, Shahin Zamani TaghizadehRabe 1 andDariushHaghmorad1,1Immunology Research Center, Bu-Ali Research Institute, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran, 2Biotechnology Research Center and School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

Study the Anti-Cancer and Anti-Inflammatory Properties of Rose Bengal in vitro, Paper 294ShahrzadZamaniTaghizadehRabe1, Mahmoud Mahmoudi1,SeyedHadiMousavi2, Maryam Rastin1, Shahin Zamani TaghizadehRabe1,NafiseTabasi1,NoushinLotfi1 and Maryam Rahnama1, 1Immunology Research Center, Bu-Ali Research Institute, School of Medicine, Mashhad University of Medical Sciences, Razavi Khorasan Province, Mashhad, Iran, 2Pharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Razavi Khorasan Province, Mashhad, Iran



The Differential Regulation of the Interferon Alpha Subtypes in Response to Viral Infection, Paper 295LunaA.ZaritskyandKathrynC.Zoon,Cytokine Biology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA

IL-17-Signaling in LGR5-Positive Stem Cells Promotes Colon Tumorigenesis, Paper 296Jarod A. Zepp1,2,CainiLiu1, Muhammet F. Gulen1,JunjieZhao1,2, Chunfang Gu1,KatarzynaBulek1andXiaoxiaLi1, 1Department of Immunology, Lerner Research Institute Cleveland Clinic Foundation, Cleveland, OH, USA, 2Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, USA

Type I Interferon in Bats: is it Special?, Paper 297Peng Zhou1*, Chris Cowled 1, James Wynne1,JustinNg1,LinfaWang1,2 and Michelle Baker 1, 1CSIRO Animal, Food and Health Sciences, Australian Animal Health Laboratory, Geelong, Victoria 3220, Australia, 2 Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, Singapore 169857, Singapore

Expression Screens Identify a Viral Bias in Interferon Effector Specificity and a Requirement for CGAS in Antiviral Immunity, Paper 298John W. Schoggins1,#,*,DonnaA.MacDuff2,NaokoImanaka1,MariaD.Gainey3,JenniferL.Eitson4,KatrinaB.Mar4, R. Blake Richardson4,ReaDabelic5,VladimirLitvak6, Alexander V. Ratushny6,7,BalajiManicassamy8, Alan Aderem6, Richard M. Elliott9, Adolfo Garcia-Sastre10,11,12, Vincent Racaniello5,EricJ.Snijder13, Wayne M. Yokoyama3,MichaelS.Diamond2,14,HerbertW.Virgin2, and Charles M. Rice1* , 1Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY 10065, 2Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, 3Rheumatology Division, Department of Medicine, and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, 4,#Present address: Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, 5Department of Microbiology and Immunology, Columbia University, New York, NY 10032, 6Seattle Biomedical Research Institute, Seattle, WA, 98109, 7Institute for Systems Biology, Seattle, WA 98109, 8Department of Microbiology, University of Chicago, Chicago, IL 60637, 9School of Biology, University of St. Andrews, St. Andrews, Scotland, UK; present address MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland , UK, 10Department of Microbiology, Icahn School of Medicine at Mt. Sinai, New York, NY, 10029, 11Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mt. Sinai, New York, NY, 10029, 12Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mt. Sinai, New York, NY, 10029, 13Department of Medical Microbiology, Leiden University Medical Center, Leiden, The Netherlands, 14Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.

Protein Tyrosine Phosphatase Non-Receptor Type 22 Potentiates Toll-Like Receptor-Driven, Type 1 Interferon-Dependent Immunity, Paper 299Yaya Wang1,4*, Iftach Shaked2*, Stephanie M. Stanford3*, Wenbo Zhou1,4, Julie M. Curtsinger4, Zbigniew Mikulski2, Zachary R. Shaheen5, Genhong Cheng6,KristySawatzke1,4, Amanda M. Campbell3,JenniferL.Auger4,10,HaticeBilgic1,4, Fernanda M. Shoyama1,4,DavidO.Schmeling7,HenryH.BalfourJr.7,KiminoriHasegawa8, Andrew C. Chan9, John A. Corbett5, Bryce A. Binstadt4,10, Matthew F. Mescher4,KlausLey2*,NunzioBottini3*, and Erik J. Peterson1,4*. 1Department of Medicine, University of Minnesota, Minneapolis, MN 55455, 2Division of Inflammation Biology, La Jolla Institute for Allergy & Immunology, La Jolla, CA 92037, 3Division of Cellular Biology, La Jolla Institute for Allergy & Immunology, La Jolla, CA 92037, 4Center for Immunology, University of Minnesota, Minneapolis, MN 55455, 5 Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, 6Department of Microbiology, Immunology & Molecular Genetics, UCLA, Los Angeles, CA 90095, 7Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455, 8Division of Rheumatology, Kin-ikyo-chuo Hospital, 10-2 Fushiko, Higashiku, Sapporo, 007-0870, Japan, 9Department of Immunology, Genentech, San Francisco, CA 94080, 10Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455 *These authors contributed equally to this work.

Systemic Blocking of the Interferon-Alpha/Beta Receptor Subunit 1 Stimulates Arteriogenesis in Mice without Affecting Atherosclerosis, Paper 300Marieke C.S. Boshuizen(1),PaulF.A.Teunissen(2),MauritsR.Hollander(2),NinaW.vanderHoeven(2), Saskia van der Velden(1), MarionJ.J.Gijbels(1),AntonJ.G.Horrevoets(3),NielsvanRoyen(2), and Menno P.J. de Winther(1), (1) Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands, (2) Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands, (3)Department of Molecular Cell biology and Immunology, VU University Medical Center, Amsterdam, the Netherlands



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“A Time to Live, a Time to Die” – The Mechanism of Interferon-Induced Apoptosis, Paper 301Amir Apelbaum, Ganit Yarden and Gideon Schreiber, Weizmann Institute of Science, Rehovot, Israel.

Suppressors of Cytokine Signaling Socs4 and Socs5 Protect against Severe Influenza Infection and Early Cytokine Storm, Paper 302LukaszKedzierski1,2,EdmondLinossi1,2,TatianaKolesnik1, Indu Chandrashekaran3,BridieDay2,NicolaBird2,TracyWilson1, James Murphy1,2, Jeffrey Babon1,2, Gabrielle Belz1,2,RaymondNorton3,NicosNicola1,2,KatherineKedzierska2, and Sandra Nicholson1,2. 1Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052; 2The University of Melbourne, Parkville, VIC 3050; 3Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.

Bioassay Development of Cytokines Involved in Neutrophil Production, Paper 303HortensiaSoto,WillieHsu,RenaChen,JuanMoyron,JohnRansom,andJieZhou,BioLegend, San Diego, California, USA

Correlating Kinetics of Lymphocyte Activation and Cytokine Secretion, Paper 304KimvanTran,JulieClor,Wen-RongLieandKamalaTyagarajan,EMD Millipore, Hayward, California USA

CXCL12 Mediates Hypoxia-Induced Connective Tissue Growth Factor Expression and Cell Differentiation in Human Lung Fibroblasts, Paper 305Bing-Chang Chen(1),Chih-ChiehTseng(2),Chi-LiChung(1),Chien-HuangLin(2), (1) School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan, (2) Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan

Involvement of Inos/No and Ros in a Reciprocal Interaction of Glioma and Microglia Cells via TNF-A and MCP-1 Production, Paper 306Shing-ChuanShen,Yi-HsuanChen,Liang-YoYang,Yen-Chou Chen*, Taipei Medical University, Taipei, Taiwan

Commensals Engage the IL-17a Inflammatory Axis to Amplify Chronic Pulmonary Inflammation, Paper 307KoshikaYadava,AurélienTrompette,EvaGollwitzer,LaurentP.Nicod,BenjaminJ.Marsland,CHUV, UNIL, Lausanne, Switzerland

IL-15.IL-15RαComplexSheddingfollowingTranspresentationisEssentialforILl-15RespondingNkandTCellSurvival, Paper 308FellaTamzalit,IsabelleBarbieux,ArianePlet,JulieHeim,Sébastien Morisseau,YannickJacquesandErwanMortier,Cancer Research Center Nantes-Angers, UMR892-INSERM 6299-CNRS, Team Cytokines and Receptors in Immuno-Oncology. University of Nantes, France

The Diagnostic and Prognostic Value of Sil-2r in Head & Neck Cancer, Paper 309Vivian Barak,K.Rachmut,M.Wigoda,T.Peretz,J.Elidan,E.Eliashar,andM.Gross,Immunology Lab for Tumor Diagnosis, Dept of ENT, Head&Neck Surgery, Hadassah -Hebrew University Medical Center, Jerusalem, Israel

Antitumor Effect of Carnosol on Regulatory CD4+ CD25+ Foxp3+ T Lymphocytes and Tumor Growth in Murine Breast Cancer Model, Paper 310ShahrzadZamaniTaghizadehRabe1, Maryam Rahnama1,BamdadRiahiZanjani2, Mahmoud Mahmoudi1, Maryam Rastin1,NafiseTabasi1 , 1 Immunology Research Center, Bu-Ali Research Institute, School of Medicine, Mashhad University of Medical Sciences, Razavi Khorasan Province, Mashhad, Iran, 2 Department of Pharmacotoxicology, School of Medicine, Mashhad University of Medical Sciences, Razavi Khorasan Province, Mashhad, Iran

Human CD1C+ Dendritic Cells Secrete High Levels of IL-12 and Potently Prime Cytotoxic T Cell Responses, Paper 311GiuliaNizzoli,JanaKrietsch,AnjaWeick,SvenjaSteinfelder,FedericaFacciotti,PaolaGruarin,AnnalisaBianco,BodoSteckel,MonicaMoro,MariaCristinaCrosti,ChiaraRomagnani,KatharinaStölzel,SaraTorretta,LorenzoPignataro,CarmenScheibenbogen,PetraNeddermann,RaffaeleDeFrancesco,SergioAbrignani,JensGeginat,INGM, Milano, ItalyThe Requirement for IL-1 in Adjuvant-Induced Inflammation is Size-Dependent, Paper 312ClaireH.A.HearndenandEdC.Lavelle,Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland

IRF7 Pathway Active in Tamoxifen Resistant Mammary Preneoplasia Induced by Either Estrogen Receptor Over-Expression or Loss of BRCA1, Paper 313KeunsooKang (1),SarahDabydeen (2),EdgarS.Diaz-Cruz (2,3) LotharHennighausen (1) and Priscilla A. Furth (2) (1) NIDDK, NIH, Bethesda, MD 20892, (2) Departments of Oncology & Medicine, Lombardi ComprehensiveCancer Center, Georgetown University, Washington, DC 20057 (3) Belmont University College of Pharmacy, Nashville, TN 37212



HMGB1, IL-8 and IL-8RA in Non-Infectious Acute Lung Injury Induced by Warm Saline Infusion in Rabbit, Paper 314CilmerySuemiKurokawa,JoseRobertoFioretto,JoãoPessoadeAraujoJúnior,RafaelleBatistellaPires,SusianedeOliveiraKlefens,MarcosMoraes,RossanoCesarBonatto,MariaReginaMoretto,LeonardoTeixeiraLopez,MarioFerreiraCarpi.Department of Pediatrics; Botucatu Medical School – Sao Paulo State University – UNESP.

CR-8 Deficiency Causes Exacerbation of Contact Hypersensitivity Due to Enhanced Dendritic Cell Migration, Paper 315Rikio Yabe,KenjiShimizu,SoichiroShimizu,SatoeAzechi,Byung-IlChoi,SachikoKubo,ShigeruKakuta,SusumuNakaeandYoichiro Iwakura, Tokyo University of Science, Noda, Japan

Effects of Pollen Lipids on Cytokine Secretion from Pbmc in Atopic and Non-Atopic Cases, Paper 316Mohammad Fereidouni andShaghayeghsadatNouranihassankiade,Asthma, Allergy & Immunology Research Center, Birjand University of Medical Sciences, Birjand, Iran

BH3 Interacting Domain Death Agonist Gene Therapy Enhances Antitumor Effect of Interferon-Alpha, Paper 317TakayaTsuno(1),ShoheiKanno(1), Joseph Bekisz(2),KathrynC.Zoon(2)andNoboruTanigawa(1), (1) Department of Radiology, Kansai Medical University, Osaka, Japan, (2) National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA

ProteinKinaseCFamilyandΘ-Subtype-SelectiveInhibitors R896 and R682 Block T Cell Activation and Protect in Experimental Models of Immune-Mediated Disease, Paper 318S.J.Holland,M.Wang,M.Duncton,A.Owyang,E.Tai,S.Yi,S.Braselmann,A.Bagos,R.Roe,G.Park,C.Choy,R.Frances,S.Siu,C.Young,J.Zhang,H.Li,P.Pine,R.Singh,D.G.Payan,andE.S.Masuda,Rigel Inc., South San Francisco, CA, USA

Development of Sandwich Immunoassays for Quantification of Total TGFß1, Free Active GFß1, Latency-Associated Peptide (Lap) and Latent TGFß in Biological Samples, Paper 319LingpuDong,TakatokuOida,JieZhou,BinggangSun,JianyongHuang,NaomiUrbina,andShaoquanJi, BioLegend, Inc., San Diego, CA 92121

Cytokines and Cellular Responses to NIPAH Virus-like Particles, Paper 320Pramila Walpita,GaryKlimpel, and Janice Endsley, University of Hawaii School of Medicine, Honolulu, Hawaii USA

Dectin-1 Signaling Synergistically Enhances Toll-Like Receptor-Mediated Production of Interferon Beta, Paper 321MotohikoKadoki,YamatoSasaki,CeTang,TomonoriKamiyaandYoichiroIwakura,Division of Experimental Animal Immunology, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Chiba, Japan.

The N-Terminus of Unc93b is Cleaved by Host and Enteroviral Proteases, Paper 322 KatharineGHarris and Carolyn Coyne, University of Pittsburgh Medical School, Pennsylvania

Chemical Genetics Reveal that Janus Kinase 3 Catalytic Activity is Required for Interleukin-2 Signal Transduction, Paper 323Geoffrey A. Smith1, Arthur Weiss2,3,andJackTaunton2,4, 1Chemistry and Chemical Biology Graduate Program, 2Howard Hughes Medical Institute, 3Division of Rheumatology, Department of Medicine, Rosalind Russell Medical Research Center for Arthritis and 4Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, USA.

Distinct Roles of IL-25 and IL-33 in Spontaneous Arthritis in Interleukin-1 Receptor Antagonist-Deficient Mice, Paper 324AyaNambu(1),KatsukoSudo(2)andSusumuNakae(1). (1) Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan, (2) Animal Research Center, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan

Proteasome Defects in Candle Patients’ Cells Lead to IFN Production in Both Hemopoietic and Non-Hemopoietic Cells, Paper 325YinLiu1,AngeliqueBiancotto2,YanHuang1, Massimo Gadina, John Philip McCoy2, Raphaela Goldbach-Mansky1.1Translational Autoinflammatory Disease Section, NIAMS, NIH, Bethesda, MD, 2Center for Human Immunology, NHLBI, NIH, Bethesda, MD. 3Office of Science and Technology, NIAMS, NIH, Bethesda, MD.

Toxoplasma Gondii-Induced Th1 Cells and Intestinal Dysbiosis Cooperate in IFN-G-Dependent Elimination of Paneth Cells, Paper 326Megan Raetz1,Sun-heeHwang1, Cara Wilhelm1, Carolyn Sturge1, Julie Mirpuri1,LoraVHooper1,2 and Felix Yarovinsky1, 1Department of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. 2The Howard Hughes Medical Institute



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Mammary-Specific Gene Activation is Defined by Progressive Recruitment of Stat5 during Pregnancy and the Establishment of H3k4me3 Marks, Paper 327KeunsooKang,DaisukeYamaji,GertraudW.Robinson,LotharHennighausen,National Institutes of Health,Bethesda, Maryland

Diagnostic Utility of Copeptin in Addition to High-Sensitivity Cardiac Troponin for the Early Diagnosis of Non-ST-Elevation Acute Coronary Syndrome,Paper 328ElenaToniato,RosaDiScala,IvanaCataldo,FabrizioRicci,DorannaDePace,RaffaeleDeCaterina,University of Chieti, Chieti, Italy

Mechanisms of Autoinhibition and Inflammasome Assembly Revealed by the Structure of the Aim2 Pyrin Domain, Paper 329TengchuanJin,AndrewPerry,PatrickSmith,JianshengJiang,andT.SamXiao,Structural Immunobiology Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA 20892-0430

TNF-Superfamily Member TL1a Elicits Type 2 Innate Lymphoid Cells at Mucosal Barriers, Paper 340Xin Yu,RajitaPappu,VladimirRamirez-Carrozzi,PatrickCaplazi,JuanZhang,DonghongYan,MinXu,WyneP.Lee,andJaneL.Grogan, Genentech, South San Francisco, California USA

Wound Healing Effects and Possible Mechanism of Action of the Butanol Fraction from Hydnocarpi Semen Crude Extract in vitro Acute Inflammation Model, Paper 331GeumSeonLee1,3,KiManLee1,3,HongShim1,3,SeungHyunKim1,3,DongSoolYim1,JaeHoonCheong1,2 and TaeJinKang1,3*, 1College of Pharmacy, Sahmyook University, Seoul, 139-742 Korea, 2 Uimyung Research Institute for Neuroscience, Sahmyook University, Seoul, 139-742 Korea, 3 Institute of Chronic Disease, Sahmyook University, Seoul, 139-742 Korea

Maternal And Fetal T Cell Responses During Normal Pregnancy And Preterm Labor, Paper 332Michela Frascoli1, 2,LacyConiglio1, 2,QizhiTang2,TippiC.MacKenzie1,2, 1Eli and Edy the Broad Center of Regeneration Medicine, 2Department of Surgery, UCSF, San Francisco, California, USA

TNF-Superfamily Member TL1a Elicits Type 2 Innate Lymphoid Cells at Mucosal Barriers, Paper 333Xin Yu1,RajitaPappu1, Vladimir Ramirez-Carrozzi1, Patrick Caplazi2, Juan Zhang3,DonghongYan3,Min Xu3,WyneP.Lee3, JaneL.Grogan1*, Departments of 1Immunology, 2Pathology and 3Translational Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080

Antigen-Specific Tolerance Requiring Regulatory T Cells, Paper 334Craig P. Chappell(1)*,NataliaV.Giltiay(1)*,KevinE.Draves(1),KevinChen(1), Mark J Shlomchik(2),DanielH.Kaplan(3), and Edward A. Clark(1) (1)DepartmentofImmunology,UniversityofWashington,Seattle,Washington,USA,(2)DepartmentofImmunology,Universityof Pittsburgh, Pittsburgh, Pennsylvania, USA and (3)DepartmentofDermatology,UniversityofMinnesota,Minneapolis,Minnesota,USA*Equalcontribution

Soluble Type I Interferon Receptor is Elevated by Interferon Treatment and in Certain Autoimmune Diseases, Paper 335TaherFatakdawala1, Michael Skawinksi1, Jonathan Ferriera2,TaraStauffer1, ThomasB.Lavoie1, 1Product Research & Development and Assay Services, PBL Assay Science, Piscataway, New Jersey, USA. 2Quality Control, PBL Assay Science, Piscataway, New Jersey, USA

8:00 – 12:00 M CYTOKINES 2013 BANQUET Grand Ballroom A Followed By Entertainment

Thursday, October 3, 2013

8:30 – 11:30 am Plenary Session IV: From Bench to Bedside Grand Ballroom A Chairs: K. Christopher Garcia, Stanford University, Palo Alto, CA, USA and James Allison,MDAnderson CancerCenter,Houston,TX,USA

8:30 – 9:00 am The Good and Evil Faces of the Janus Kinases: Implications for Immunotherapy, Paper S-26 TomWaldmann,NationalCancerInstitute,NIH,Bethesda,MD,USA

International Cytokine and Interferon SocietyInternational Cytokine and Interferon Society


9:00 – 9:30 am Control of Cytokine Inflammation TakMak,UniversityofToronto,Ontario,Canada

9:30 – 10:00 am Complexity of Cytokines in Treg Function and Stability, Paper S-1 Jeff Bluestone; University of California, San Francisco, CA, USA 10:00 – 10:30 am A Novel IL-6 mRNA Stability Protein, Arid5A which is involved in IL-6 Dependent Autoimmunity, Paper S-5 TadamitsuKishimoto,OsakaUniversity,Osaka,Japan

10:30 – 11:00 am The Beta Common Cytokine Receptor Family: Structural Insights and Signaling Mechanisms, Paper S-28 AngelLopez,CentreforCancerBiology,SAPathology,Victoria,Australia

11:00 – 11:30 am Immune Checkpoint Blockade in Cancer Therapy: New Insights and Opportunities JamesAllison.UniversityofTexasMDAndersonCancerCenter,Houson,TX,USA

11:30 am CLOSING REMARKS WarrenLeonard

Note:10:00-10:45am-CoffeeAvailable–GrandBallroomFoyer


Thurssday, October 3, continued

ABSTRACTSMINISYMPOSIUM 6: Abstracts 298 & 299

298EXPRESSION SCREENS IDENTIFY A VIRAL BIAS IN INTERFERON EFFECTOR SPECIFICITY AND A REQUIREMENT FOR CGAS IN ANTIVIRAL IMMUNITY.John W. Schoggins1,#,*, Donna A. MacDuff2, Naoko Imanaka1, Maria D. Gainey3, Jennifer L. Eitson4, Katrina B. Mar4, R. Blake Richardson4, Rea Dabelic5, Vladimir Litvak6, Alexander V. Ratushny6,7, Balaji Manicassamy8, Alan Aderem6, Richard M. Elliott9, Adolfo Garcia-Sastre10,11,12, Vincent Racaniello5, Eric J. Snijder13, Wayne M. Yokoyama3, Michael S. Diamond2,14, Herbert W. Virgin2, and Charles M. Rice1* , 1Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY 10065, 2Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, 3Rheumatology Division, Department of Medicine, and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, 4,#Present address: Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, 5Department of Microbiology and Immunology, Columbia University, New York, NY 10032, 6Seattle Biomedical Research Institute, Seattle, WA, 98109, 7Institute for Systems Biology, Seattle, WA 98109, 8Department of Microbiology, University of Chicago, Chicago, IL 60637, 9School of Biology, University of St. Andrews, St. Andrews, Scotland, UK; present address MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland , UK, 10Department of Microbiology, Icahn School of Medicine at Mt. Sinai, New York, NY, 10029, 11Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mt. Sinai, New York, NY, 10029, 12Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mt. Sinai, New York, NY, 10029, 13Department of Medical Microbiology, Leiden University Medical Center, Leiden, The Netherlands, 14Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.The type I interferon (IFN) response protects cells from invading viral pathogens by triggering the transcription of interferon-stimulated genes (ISGs). Although hundreds of ISGs have been identified, relatively few have been characterized with respect to antiviral activity. For most, little is known about their antiviral potential, their target specificity, and their mechanisms of action. We have established an overexpression screening platform to evaluate the antiviral potential of more than 350 ISGs against a diverse panel of animal viruses spanning the viral

phylogeny. To date, we have screened 14 plus-strand RNA viruses, 7 negative-strand RNA viruses, and one DNA virus. Hierarchical clustering of top ISG hits showed that viruses segregate based on their genomic content, with plus-stranded RNA viruses exhibiting the highest sensitivity to the greatest number of ISGs. Gene clustering revealed cyclic GMP-AMP synthase (cGAS, also known as MB21D1) as having broad antiviral activity, consistent with recent studies showing that this protein is a newly discovered viral sensor. In vitro studies indicate that enzymatically active cGAS activates a generalized STING-dependent, IRF-3-mediated antiviral program that can function independently of canonical IFN/STAT1 signalling. We have also generated cGAS (Mb21d1) knockout mice and demonstrate that cGAS is required for optimal antiviral responses to DNA viruses. Collectively, our studies uncover new paradigms for the specificity of interferon-mediated innate antiviral pathways and highlight a critical role for cGAS in controlling viral infections in vivo.

299 Protein Tyrosine Phosphatase Non-Receptor Type 22 Potentiates Toll-Like Receptor-Driven, Type 1 Interferon-Dependent Immunity.Yaya Wang1,4*, Iftach Shaked2*, Stephanie M. Stanford3*, Wenbo Zhou1,4, Julie M. Curtsinger4, Zbigniew Mikulski2, Zachary R. Shaheen5, Genhong Cheng6, Kristy Sawatzke1,4, Amanda M. Campbell3, Jennifer L. Auger4,10, Hatice Bilgic1,4, Fernanda M. Shoyama1,4, David O. Schmeling7, Henry H. Balfour Jr.7, Kiminori Hasegawa8, Andrew C. Chan9, John A. Corbett5, Bryce A. Binstadt4,10, Matthew F. Mescher4, Klaus Ley2*, Nunzio Bottini3*, and Erik J. Peterson1,4*. 1Department of Medicine, University of Minnesota, Minneapolis, MN 55455, 2Division of Inflammation Biology, La Jolla Institute for Allergy & Immunology, La Jolla, CA 92037, 3Division of Cellular Biology, La Jolla Institute for Allergy & Immunology, La Jolla, CA 92037, 4Center for Immunology, University of Minnesota, Minneapolis, MN 55455, 5 Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, 6Department of Microbiology, Immunology & Molecular Genetics, UCLA, Los Angeles, CA 90095, 7Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455, 8Division of Rheumatology, Kin-ikyo-chuo Hospital, 10-2 Fushiko, Higashiku, Sapporo, 007-0870, Japan, 9Department of Immunology, Genentech, San Francisco, CA 94080, 10Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455 * These authors contributed equally to this work.Immune cells sense microbial products through Toll-like receptors (TLR), which trigger host defense responses including type 1 interferons (IFNs) secretion. A coding polymorphism in the protein tyrosine phosphatase non-


INTERNATIONAL CYTOKINE SOCIETY 11

receptor type 22 (PTPN22) gene is a susceptibility allele for human autoimmune and infectious disease. We report that Ptpn22 selectively regulated type 1 IFN production after TLR engagement in myeloid cells. Ptpn22 promoted host antiviral responses, and was critical for TLR agonist-induced, type 1 IFN-dependent suppression of inflammation in colitis and arthritis. PTPN22 directly associated with TNF receptor-associated factor 3 (TRAF3) and promotes TRAF3 lysine 63-linked ubiquitination. The disease-associated PTPN22W variant failed to promote TRAF3 ubiquitination, type 1 IFN upregulation, and type 1 IFN-dependent suppression of arthritis. The findings estab-lish a candidate innate immune mechanism of action for a human autoimmunity “risk” gene in the regulation of host defense and inflammation.

POSTER ABSTRACTS 300-335

300SYSTEMIC BLOCKING OF THE INTERFERON-ALPHA/BETA RECEPTOR SUBUNIT 1 STIMULATES ARTERIOGENESIS IN MICE WITHOUT AFFECTING ATHEROSCLEROSIS.Marieke C.S. Boshuizen(1), Paul F.A. Teunissen(2), Maurits R. Hollander(2), Nina W. van der Hoeven(2), Saskia van der Velden(1), Marion J.J. Gijbels(1), Anton J.G. Horrevoets(3), Niels van Royen(2), and Menno P.J. de Winther(1), (1) Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands, (2) Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands, (3)Department of Molecular Cell biology and Immunology, VU University Medical Center, Amsterdam, the Netherlands.Increased expression of interferon-beta (IFN-β) was shown in patients with insufficient coronary collater-alization. Furthermore, mice treated with IFN-β dem-onstrate inhibition of collateral artery growth, known as arteriogenesis. IFN-β is also involved in atheroscle-rosis and in atherosclerotic mouse models, IFN-β treatment accelerated lesion formation and increased macrophage accumulation in plaques. We hypothe-sized that inhibiting IFN-β signaling stimulates arte-riogenesis without enhancing atherosclerosis. Acceleration of atherosclerosis is an important limita-tion of pro-arteriogenic compounds investigated to date. To study our hypothesis, an atherosclerotic hindlimb-ischemia model was used in which female LDLR-/- mice were fed a high fat diet for 8 weeks. Four weeks after start of the diet, the right femoral artery was ligated after which the mice received repeated intraperitoneal injections of a monoclonal antibody specific for murine Interferon-α/β Receptor subunit 1 (IFNAR1) or murine IgG isotype as a con-trol. Reperfusion was measured using laser Doppler perfusion imaging (LDPI) directly after ligation, as

well as at 2, 7, 14 and 28 days following ligation. We also investigated the effect of anti-IFNAR1 on athero-sclerosis, which was assessed by histological analyses in the aortic root to determine total plaque area and phenotype. We observed that reperfusion after ligation was significantly improved in mice treated with anti-IFNAR1 compared to controls after 7, 14 and 28 days (treatment vs. control; 7 days: 35.6 ± 16.5% vs. 23.6 ± 8.7%, p=0.027; 14 days: 51.4 ± 17.2% vs. 35.0 ± 12.3%, p 0.010; 28 days 71.5 ± 13.8% vs. 54.0 ± 16.3%, p=0.005). Total atherosclerotic plaque area (treatment vs. control: 11.9 ± 1.2x104 μm2 vs. 13.9 ± 1.4x104 μm2, p=0.275) as well as plaque phenotype were unaffected. These data demonstrate that blocking IFNAR1 stimulates collateral artery growth in mice while having a neutral effect on atherosclerosis. Targeting IFN-β signaling might thus lead to a thera-peutic approach in stimulating arteriogenesis. This work was supported by the Dutch Heart Foundation, grant #2010B022

301“A TIME TO LIVE, A TIME TO DIE” – THE MECHANISM OF INTERFERON-INDUCED APOPTOSISAmir Apelbaum, Ganit Yarden and Gideon SchreiberWeizmann Institute of Science, Rehovot, Israel.Interferons induce a pleiotropy of responses through binding the same cell surface receptor. Here we investigated the molecular mechanism driving interferon-induced apoptosis. Apoptosis-related genes such as the caspase-8, cFLIP, and DR5 are required for interferon-induced apoptosis, which found to be independent of the activity of death ligands. Interestingly, cFLIP silencing shortened the time of apoptosis initiation from days to hours and increased dramatically the population of apoptotic cells. Thus, cFLIP serves as a timer regulator for interferon-induced apoptosis. Moreover, IFN signaling mediates fast nuclear export of cFLIP to the cytoplasm, where it blocks caspase-8 activation in the early hours of stimulation. Following prolonged IFN stimulation, caspase-8 translation increases resulting a shift in the balance between cFLIP and caspase-8 leading to downstream caspase activation and apoptosis. While type II interferon (IFN-γ) also causes caspase-8 upregulation, cFLIP nuclear export is unique for type I IFNs suggesting that it follows a different path to apoptosis.

302SUPPRESSORS OF CYTOKINE SIGNALING SOCS4 AND SOCS5 PROTECT AGAINST SEVERE INFLUENZA INFECTION AND EARLY CYTOKINE STORMLukasz Kedzierski1,2, Edmond Linossi1,2, Tatiana Kolesnik1, Indu Chandrashekaran3, Bridie Day2, Nicola Bird2, Tracy Wilson1, James Murphy1,2, Jeffrey Babon1,2, Gabrielle Belz1,2, Raymond Norton3, Nicos Nicola1,2, Katherine Kedzierska2, and


Sandra Nicholson1,2. 1Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052; 2The University of Melbourne, Parkville, VIC 3050; 3Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.Influenza is a highly infectious, acute respiratory dis-ease that causes profound morbidity and mortality. The development of a “cytokine storm” coupled with damage to pulmonary epithelium has been consistent-ly observed in severe cases of influenza infection in humans. The mechanisms underlying this pathology and an understanding as to why some individuals respond excessively to virus, remains relatively unex-plored. Cytokine binding to receptor triggers a JAK-STAT signaling cascade, which orchestrates an intri-cate series of transcriptional and cellular changes. The suppressors of cytokine signaling (SOCS) proteins (SOCS1-7 and CIS) are key physiological regulators of the cytokine networks and consequently, of innate and adaptive immunity. While the biochemical and biological functions of SOCS1-3 and CIS are well characterised, comparatively little is known regarding the biological role of SOCS4 and SOCS5. We demon-strate that mice lacking either SOCS5 or a functional SOCS4 protein (Socs4mut), rapidly succumb to infec-tion with a pathogenic H1N1 influenza virus (PR8). The increased morbidity is associated with dramati-cally greater weight loss, most likely due to elevated pro-inflammatory cytokine and chemokine production in the lungs. In addition, the mice exhibit delayed viral clearance and in Socs4mut mice this was associ-ated with impaired trafficking of influenza-specific CD8+ T cells to the site of infection and defects in T cell receptor activation. Interestingly, biochemical analysis suggests that both proteins can interact with JAK via a conserved region in the N-terminus. However, these two proteins are likely to differential-ly regulate cytokine signaling, with SOCS5 (and not SOCS4) selectively able to inhibit JAK1 and JAK2 kinase activity. These results demonstrate that SOCS4 and SOCS5 are critical regulators of anti-viral immu-nity and reveal a novel role for SOCS4 as a positive regulator of T cell signalling.

303BIOASSAY DEVELOPMENT OF CYTOKINES INVOLVED IN NEUTROPHIL PRODUCTION. Hortensia Soto, Willie Hsu, Rena Chen, Juan Moyron, John Ransom, and Jie Zhou, BioLegend, San Diego, California, USAMyelopoiesis (production of monocytes and granulo-cytes) is the major activity of the bone marrow. Hematopoietic stem cells (HSC) are surrounded by a highly regulated environment. Primitive HSCs are located in the bone marrow endosteum niche, and more mature HSC dividing cells are in the vascular or sinusoidal niche. Different cells form and regulate the

endosteal niche, such as osteoblasts, osteoclasts, mes-enchymal stromal cells (MSCs), Tregs, and mac-rophages. In the sinusoidal niche, the HSC interact with sinusoidal endothelial cells and leptin receptor+ perivascular stromal cells. Myeloid cells are derived from multipotent hematopoietic stem cells (MPC) that will be differentiated to common myeloid progenitors (CMP), and subsequently to granulocyte macrophage precursors (GMP). The key regulator of granulopoie-sis is G-CSF that regulates the production of commit-ted-myeloid progenitors. GM-CSF, IL-3, and IL-6 can stimulate granulopoiesis in vivo. IL-17-mediated gran-ulopoiesis via G-CSF induces neutrophilia. IL-17 pro-duction is induced by IL-23 in neutrophil regulatory T cells (Tn,γ δ TCR); thus, IL-23 has a role in neutro-phil homeostasis. CXCL12/SDF-1 is produced consti-tutively by bone marrow stromal cells and binds to CXCR4; this ligand-receptor pair plays a key role in neutrophil release from the bone marrow. G-CSF induces downregulation of CXCL12 and upregulation of CXCL1 and CXCL2, thereby regulating release of bone marrow neutrophils. The bioassays for cytokines involved in neutrophil production are described in this work. IL-3 and IL-6 activities were measured by induction of MNFS60 and 7TD-1 cell proliferation, respectively. IL-17A and IL-23 activities were mea-sured by their ability to induce IL-6 in dermal fibro-blasts and IL-17 in T cells, respectively. GM-CSF and G-CSF activities were measured by induction of FDC-P1 and MNFS60 cell proliferation, respectively. CXCL1/CXCL2 and CXCL12 activities were mea-sured by chemotaxis of neutrophils and T cells, respectively. We conclude that we have successfully expressed and purified multiple cytokines, and showed that they have potent biological activity.304CORRELATING KINETICS OF LYMPHOCYTE ACTIVATION AND CYTOKINE SECRETION.Kimvan Tran, Julie Clor, Wen-Rong Lie and Kamala Tyagarajan, EMD Millipore, Hayward, California USAActivation status of lymphocyte can provide critical information regarding immune response, cytokine secretion and cellular proliferation characteristics. Multiple markers are expressed on the surface of acti-vated lymphocytes. Correlations between activation-specific cell surface markers and cytokine secretion in general is well established; however, the study of kinetics of particular activation markers with broad panel of cytokines has been limited. In this study we investigated the kinetics of lymphocyte activation with the kinetics of secretion of a broad panel of cytokines. PBMC’s from multiple donors were treated with the polyclonal activator, phytohaemagglutinin or phorbol myristate acetate and ionomycin at different time intervals. Lymphocyte activation information was obtained on the Muse™ Cell Analyzer using acti-vation assays that provided information on the per-


centage of lymphocytes with CD69 and CD25 expres-sion. Information on the secretion levels of multiple cytokines was obtained utilizing a MILLIPLEX® MAP Human Th17 Magnetic Bead Panel using the Luminex® MAGPIX® System which assayed the expression levels of 25 cytokines simultaneously. Our results demonstrated that PHA activation results in significant cytokine secretion at 6 hours with almost saturating levels of secretion of IL-6, IL-1beta, TNF- alpha, which parallels CD69 expression levels. Cytokines such as IFN-gamma, IL-10, IL-2 and IL-27 are low at 6 hours but increase significantly at 24 and 48 hours after treatment paralleling expression of CD25 on the surface of lymphocytes. PMA/ionomy-cin showed different kinetics of expression of activa-tion markers for the same donors with high CD69 expression but negligible CD25 expression at 6 hours. The onset of IL-17F, IL-9 and TNF-beta secretion trended better with the level of CD25 expression on the lymphocytes. The parallel measurements of acti-vation markers at the cellular level and secreted cytokines can provide better benchmarking and under-standing of cellular changes and relationship to spe-cific cytokines in response to polyclonal stimuli.

305CXCL12 MEDIATES HYPOXIA-INDUCED CONNECTIVE TISSUE GROWTH FACTOR EXPRESSION AND CELL DIFFERENTIATION IN HUMAN LUNG FIBROBLASTS. Bing-Chang Chen(1), Chih-Chieh Tseng(2), Chi-Li Chung(1), Chien-Huang Lin(2), (1) School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan, (2) Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.Chronic lung diseases including asthma are character-ized by the airway remodeling, lung fibrosis, and hypoxia. Previous study indicated that hypoxia plays a critical role in tissue fibrosis. In chronic asthma, the CXCL12 (stromal cell-derived factor-1, SDF-1)/CXCR4 axis plays important role in pulmonary fibro-sis. In this study, we investigated the mechanisms of CXCL12 mediating hypoxia-induced CTGF expres-sion and cell differentiation in human lung fibroblasts. We found that hypoxia induced increase in CXCL12 release in time- and concentration-dependent manners. Hypoxia-induced CXCL12 release were inhibited by c/EBPβ small interfering RNA (siRNA), p300siRNA, anacardic acid (a p300 inhibitor), LY 294002 (PI3K inhibitor), and AktDN. Hypoxia caused time-depen-dent increase in c/EBPβ acetylation, p300 phosphory-lation, and Akt phosphorylation. Furthermore, hypoxia induced connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA, a myofibroblast marker) expression in human lung fibroblasts. We also found that CXCL12-induced time and concentration-dependent increase in CTGF expression and CTGF-

luciferase activity. CXCL12-induced CTGF expres-sion was inhibited by CXCR4 siRNA, AMD3100 (CXCR4 antagonist), LY 294002, and Akt DN. Furthermore, CXCL12 induces increase in α-SMA expression in a time- dependent manner; this effect was inhibited by CTGF siRNA. These results imply that hypoxia induced increase in CXCL12 release through PI3K/Akt, p300, and c/EBPβ signal pathways and CXCL12/CXCR4 axis play an important role in CTGF expression. Finally, hypoxia induced CTGF expression and cell differentiation by inducing CXCL12 release and autocrine signaling in human lung fibroblasts.

306INVOLVEMENT OF INOS/NO AND ROS IN A RECIPROCAL INTERACTION OF GLIOMA AND MICROGLIA CELLS VIA TNF-A AND MCP-1 PRODUCTION.Shing-Chuan Shen, Yi-Hsuan Chen, Liang-Yo Yang, Yen-Chou Chen*, Taipei Medical University, Taipei, TaiwanThe tumor microenvironment plays a critical role in glioblastoma invasion and progression, and microglia is one of the most abundant immune cells in the tumor. Using transwell co-culture methods with glioma cells (U87 and C6) and microglia cells BV-2, increased migration of glioma cells U87 and C6 by microglia BV2 cells or NO donor sodium nitro prusside (SNP) accompanied by increased NO production was observed, and BV2 co-culture-induced migration of U87 and C6 was blocked by adding a nitric oxide synthase (NOS) inhibitor N-nitro L-arginine methyl ester (NAME). The conditioned mediums (CM) derived from both glioma cells U87 and C6 (U87-CM and C6-CM) were prepared, CMs from glioma cells significantly induced iNOS protein and NO production cells in according with an occurrence of activated macrophages and without alternations in cell viability and cell cycle progression in microglia BV2. ERK inhibitor U0126 and JNK inhibitor SP600125 suppressed U87-CM and C6-CM-induced iNOS/NO production with respectively blocking phosphorylated ERK (pERK) and JNK (pJNK) protein expression stimulated by U87-CM and C6-CM. A significant increase in intracellular peroxide by U87-CM and C6-CM was detected via DCHF-DA assay, and vitamin C (Vit C) and N-acetyl cysteine (NAC)-reduced intracellular peroxide levels with inhibition of iNOS/NO production and pERK/pJNK protein stimulated by U87-CM and C6-CM were identified in BV-2 cells. Contribution of ROS, pERK, and pJNK to the migration of glioma cells was further demonstrated in the transwell co-culture system of glioma U87 and C6 with microglia BV-2 cells. Furthermore, TNF-a, MCP-1, CSF-1, and TGF-b were applied, and TNF-a and MCP-1 induced iNOS protein expression in time and concentration-


dependent manners, and expression of TNF-a and MCP-1 mRNA in U87 and C6 cells were detected by RT-PCR. Neutralization of TNF-a or MCP-1 in U87-CM and C6-CM using TNF-a or MCP-1 antibody inhibited iNOS protein expression, and increased intracellular peroxide by TNF-a or MCP-1 was identified in BV2 cells. The reciprocal activation of glioma cells and microglia via ROS-dependent iNOS/NO elevation at least in part mediated by TNF-a and MCP-1 is elucidated.

307COMMENSALS ENGAGE THE IL-17A INFLAMMATORY AXIS TO AMPLIFY CHRONIC PULMONARY INFLAMMATIONKoshika Yadava, Aurélien Trompette, Eva Gollwitzer, Laurent P. Nicod, Benjamin J. Marsland, CHUV, UNIL, Lausanne, SwitzerlandChanges in the bacterial microbiota are associated with chronic lung diseases such as chronic obstructive pulmonary disease (COPD). However whether there is a direct link between this phenomenon and disease progression are unknown. To address this question we have utilized a murine model that reproduces key pathological features characteristic of COPD in humans, such as emphysema, airway inflammation and progressive decline in lung function. Comparing the disease in specific pathogen free mice (SPF) and mice lacking a microbiota (germ-free), we found that the absence of a microbiota ameliorated disease, exhibited by a reduction in airway inflammation and an improvement in lung function. Moreover the absence of a microbiota resulted in an impaired pro-duction of IL-17A, a cytokine that has been implicat-ed in the pathogenesis of the human disease. Similar to human disease, in our model the kinetics of micro-biota-dependent IL-17A production correlated with the progression in the decline of lung function. Based on these data we neutralized IL-17A in SPF mice and found this treatment ameliorated disease and restored lung function to a level similar to germ-free mice. Collectively, our data demonstrates that signals from the microbiota enhance chronic lung inflammation through an IL-17A-dependent pathway, potentially highlighting two avenues of future therapeutic inter-vention against COPD.

308IL-15.IL-15Rα COMPLEX SHEDDING FOLLOWING TRANSPRESENTATION IS ESSENTIAL FOR IL-15 RESPONDING NK AND T CELL SURVIVALFella Tamzalit, Isabelle Barbieux, Ariane Plet, Julie Heim, Sébastien Morisseau, Yannick Jacques and Erwan Mortier, Cancer Research Center Nantes-Angers, UMR892-INSERM 6299-CNRS, Team Cytokines and Receptors in Immuno-Oncology. University of Nantes, France.

Interleukin-15 (IL-15), a member of the four α helix bundle family of cytokines has emerged as a promis-ing agent for cancer immunotherapy. IL-15 plays an important role in innate and adaptive immunity as it acts on the early stages of T and NK cells differentia-tion and activation, as well as on the survival of mem-ory CD8 T cells. IL-15 signals are delivered via a het-erotrimeric receptor complex composed of a private chain IL-15Rα, the IL-15/IL-2Rβ and the common γ chain. IL-15 can act directly on the trimeric receptor via cis-presentation or by another specific mechanism of action called trans-presentation by which IL-15 bound to IL-15Rα on presenting cells can activate the transduction receptor complex IL-15Rβ/γ expressed on NK and T cells. IL-15Rα undergoes proteolytic cleavage and is released into the surrounding environ-ment as a soluble receptor that is bound or not to IL-15. The advantage of this cleavage is still unclear. Indeed, the soluble receptor sIL-15Rα can act as an antagonist of IL-15 or as an agonist according to the targeted cells. Aim: Our aim was to study the role of IL-15.IL-15Rα shedding after trans-presentation. Methods: Using molecular biology, we generated an uncleavable form of human IL-15Rα by deleting the sequence, which is close to the membrane. Having an uncleavable form of IL-15Rα allowed us to study the role of this process in the regulation of NK and T cells activation and survival. Results: In this study we have shown that following trans-presentation, IL-15.IL-15Rα complex is cleaved from surface presenting cells and internalized within NK and T responding cells. This process allows responding cells to reuse the internalized IL-15.IL-15Rα for residual prolifera-tion. Conclusion: Our study demonstrates a novel mechanism regulating IL-15 trans-presentation and refines our understanding of cytokines delivery regu-lation.

309THE DIAGNOSTIC AND PROGNOSTIC VALUE OF sIL-2R in HEAD & NECK CANCER.Vivian Barak, K. Rachmut, M.Wigoda, T.Peretz, J. Elidan, E.Eliashar, and M.Gross, Immunology Lab for Tumor Diagnosis, Dept of ENT, Head&Neck Surgery, Hadassah -Hebrew University Medical Center, Jerusalem, Israel. Aims: To evaluate whether soluble IL-2 Receptor (sIL-2R) levels can serve as potential biomarkers for diagnosis, assessing treatment response and prognosis in Head & Neck (H&N) Cancer patients (Ca pts).Methods: We have assessed 120 H&N Ca pts pre and post-surgery. In addition, 20 healthy age-and sex-matched controls were included. Correlations of sIL-2R levels (medians) to grade, stage, lymph node involvement and pathology, were performed. Levels of sIL-2R in pts sera were evaluated by an ELISA assay. Results: Serum levels (medians) of sIL-2R after surgery were lower than before (963 ± 65 vs.


697± 108).p=0.05.Higher levels were found in T4 compared to T1, T2 and T3 pts (1073 ± 122 vs. 671 ± 52, p=0.02). Nodal disease was accompanied with higher sIL-2R levels compared to negative nodal dis-ease (1013 ± 187 vs. 686 ± 73, p=0.04). In poorly dif-ferentiated Cancer, levels of sIL-2R were significantly higher (1377 ± 55 vs. 777± 37, p=0.001) than in well differentiated Cancers. According to ROC analysis, sIL-2R levels distinguished by 90% between H&N Ca pts and normal controls, by a cut off point of 533 u/ml.A significant correlation (Spearman Coefficient of Correlation) was demonstrated between response to therapy, survival and sIL-2R levels which decreased, accordingly, r = 0.5086 (P<0.0001). Conclusions: High sIL-2R levels may distinguish between H&N Ca pts and healthy individuals. Higher sIL-2R levels cor-relate to a higher grade and to poorly differentiated H&N Cancer. A better survival rate was attributed to pts with lower levels of sIL-2R. Taken together, we demonstrated sIL-2R, as an immune biomarker, asso-ciated with diagnosis, therapy response, prognosis and survival in H&N Cancer pts.

310ANTITUMOR EFFECT OF CARNOSOL ON REGULATORY CD4+ CD25+ Foxp3+ T LYMPHOCYTES AND TUMOR GROWTH IN MURINE BREAST CANCER MODELShahrzad Zamani Taghizadeh Rabe1, Maryam Rahnama1, Bamdad Riahi Zanjani2, Mahmoud Mahmoudi1, Maryam Rastin1, Nafise Tabasi 1 , 1 Immunology Research Center, Bu-Ali Research Institute, School of Medicine, Mashhad University of Medical Sciences, Razavi Khorasan Province, Mashhad, Iran, 2 Department of Pharmacotoxicology, School of Medicine, Mashhad University of Medical Sciences, Razavi Khorasan Province, Mashhad, Iran.Carnosol is an ortho-diphenolic diterpene which is found in natural sources such as Rosmarinus officina-lis L. and is considered as a promising anti-cancer and anti-inflammatory agent. In the present research we evaluated effect of Carnosol administration on tumor size and immune responses in both spleen and tumor. For this purpose, we developed BALB/c mouse model by injection of WEHI-164 fibrosarcoma cells. Carnosol (5 and 10 mg/kg), rapamycin (1.5 mg/kg) and cyclophosphamide (20 mg/kg) were intraperitone-ally administered for 7 days and tumor sizes were measured every other day. Then, mice were sacrificed and mononuclear cells were isolated from both spleens and tumors. Splenocyte proliferation detected using MTT assay and cytokine profile was assessed by ELISA. Moreover, T-lymphocytes subpopulation and regulatory CD4+CD25+Foxp3+ T lymphocytes in tumor-infiltrated and spleen lymphocytes were ana-lyzed by Flow cytometry. Our findings showed a sig-nificant decrease in the tumor volume and the level of

IL-4 and IL-10 and a significant increase in spleno-cyte proliferation and the level of IFN-γ in the mice treated with Carnosol, rapamycin and cyclophosph-amide, compared to untreated group. Furthermore, administration of carnosol has resulted in a significant reduction in regulatory CD4+CD25+Foxp3+ T lym-phocytes. Our results provide more evidences on the anticancer potential of Carnosol. Moreover, involve-ment of immune responses as mechanism of action of Carnosol was revealed.

311HUMAN CD1C+ DENDRITIC CELLS SECRETE HIGH LEVELS OF IL-12 AND POTENTLY PRIME CYTOTOXIC T CELL RESPONSES.Giulia Nizzoli, Jana Krietsch, Anja Weick, Svenja Steinfelder, Federica Facciotti, Paola Gruarin, Annalisa Bianco, Bodo Steckel, Monica Moro, Maria Cristina Crosti, Chiara Romagnani, Katharina Stölzel, Sara Torretta, Lorenzo Pignataro, Carmen Scheibenbogen, Petra Neddermann, Raffaele DeFrancesco, Sergio Abrignani, Jens Geginat,INGM, Milano, ItalyDendritic cells (DC) have the unique capacities to induce primary T cell responses. In mice, CD8a+DC are specialised to cross-prime CD8+ T-cells and pro-duce IL-12 that promotes cytotoxicity. Human BDCA-3+DC share several relevant characteristics with CD8a+DC, but the capacities of human DC sub-sets to induce CD8+ T cell responses are incompletely understood. We compared CD1c+mDC1, BDCA-3+mDC2 and plasmacytoid DC (pDC) in peripheral blood and lymphoid tissues for phenotype, cytokine production and their capacities to prime cytotoxic T cells. mDC1 were surprisingly the only human DC that secreted high amounts of IL-12p70, but they required combinational Toll-like receptor (TLR) stim-ulation. mDC2 and pDC produced IFN-l and IFN-a, respectively. Importantly, mDC1 and mDC2 required different combinations of TLR-ligands to cross-pres-ent protein antigens to CD8+ T cells. pDC were ineffi-cient, and also expressed lower levels of MHC- and co-stimulatory molecules. Nevertheless, all DC induced CD8+ memory T-cell expansions upon licens-ing by CD4+ T cells, and primed naive CD8+ T-cells following appropriate TLR stimulation. However, since mDC1 produced IL-12 they induced the highest levels of cytotoxic molecules. In conclusion, CD1c+mDC1 are the relevant source of IL-12 for naïve T cells, and are fully equipped to cross-prime cytotoxic T cell responses.

312THE REQUIREMENT FOR IL-1 IN ADJUVANT-INDUCED INFLAMMATION IS SIZE-DEPENDENT.Claire H.A. Hearnden and Ed C. Lavelle, Trinity Biomedical Sciences Institute, Trinity College Dublin,


Dublin 2, Ireland. Advances in vaccine development have enabled the use of subunit vaccines which do not use whole organisms but instead incorporate specific antigens into formulations containing adjuvants. Many particu-late adjuvants are known to induce an IL-1-dependent inflammatory response at the site of injection. Since particulate adjuvant size is known to influence adap-tive immunity, and the innate immune response deter-mines the nature of the ensuing adaptive immune response, we wanted to determine whether size plays a role in regulating IL-1 signalling and innate immune responses in vivo. Firstly, the inflammatory profile of mice immunised intraperitoneally with polystyrene particles ranging in size from 50nm-100µm was deter-mined. 50nm and 10µm particles were the most inflammatory stimuli, inducing the local production of IL-1β as well as the chemoattractants KC and MIP-2 and recruiting neutrophils and M1-like macrophages into the site of injection. 50nm particles also induced the production of IL-33 and the recruitment of eosino-phils. In contrast, injection of 100µm PS particles elicited limited inflammation. Particles of between 50nm and 10µm in size have previously been shown to promote NLRP3 inflammasome-dependent secre-tion of IL-1β by dendritic cells in vitro. However, although several groups have shown that particulates such as alum, silica crystals and monosodium urate crystals induce IL-1R-dependent recruitment of neu-trophils, the role for IL-1 in particle-induced inflam-mation in vivo is unclear. Although neutrophil recruit-ment in response to 50nm PS particles was IL-1R-dependent, 10µm PS particle-induced neutrophil recruitment was IL-1R-independent. Remarkably, micro-particles induce the secretion of IL-1β both sys-temically and locally, yet it is dispensable for the sub-sequent recruitment of neutrophils. This study indi-cates a novel size-dependent role for IL-1 in particle-induced neutrophil recruitment that has not previously been demonstrated.

313IRF7 PATHWAY ACTIVE IN TAMOXIFEN RESISTANT MAMMARY PRENEOPLASIA INDUCED BY EITHER ESTROGEN RECEPTOR OVER-EXPRESSION OR LOSS OF BRCA1.Keunsoo Kang (1), Sarah Dabydeen (2), Edgar S. Diaz-Cruz (2,3) Lothar Hennighausen (1) and Priscilla A. Furth (2)(1) NIDDK, NIH, Bethesda, MD 20892, (2)

Departments of Oncology & Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057 (3) Belmont University College of Pharmacy, Nashville, TN 37212. Development of tamoxifen resistance is a well-recog-nized clinical problem in the treatment of established breast cancer. There is evidence that genetic factors

can influence tamoxifen susceptibility in women who receive tamoxifen as a primary or secondary preven-tive. Here RNA-seq was applied to three genetically engineered mouse (GEM) models of breast cancer in conjunction with wild-type (WT) mice to identify a candidate mammary preneoplasia transcriptome pre-dictive of tamoxifen resistant mammary preneoplasia. Two of the GEM models, ERa over-expression (tet-op-Esr1MMTV-rtTA mice) and Brca1 deficiency coupled with p53 haploinsufficiency (Brca1f11/f11/MMTV-Cre/p53+/- mice) are characterized by tamoxifen resistance while one of the GEM models, aromatase over-expression (tet-op-CYP19A1MMTV-rtTA mice), demon-strates tamoxifen sensitivity. RNA libraries were pre-pared from the mammary tissue of untreated 12 month-old-mice followed by deep sequencing. Transcript abundance (FPKM, Fragments Per Kilobase of transcript per Million mapped reads) and differentially expressed genes (DEGs) were deter-mined after assembling transcriptomes using Cufflinks. DEGs were defined as genes showing 2-fold up- or down-regulated expression in both sin-gle- and paired-end data. Totals of 291, 837 and 359 DEGs were identified in mice with ERa over-expres-sion, Brca1 deficiency and aromatase over-expression, respectively compared to WT mice. Gene Ontology and network analyses were performed using ClueGO, GeneMANIA and MCODE via the Cytoscape net-work analysis platform. Motif analysis was performed using Pscan with the JASPAR motif database and coding potential evaluated using CPAT. Genes associ-ated with immune system processing (68 genes) were up-regulated in tamoxifen-resistant ERa over-express-ing and Brca1 deficient mice whereas genes related to aromatic compound metabolic process were up-regu-lated in tamoxifen-sensitive aromatase over-express-ing mice. Irf7 (Interferon Regulatory Factor 7) was identified as a key transcription factor regulating these 68 immune processing genes. In addition two loci encoding novel transcripts with high homology to Human, Rabbit and Cow IGLL1 were uniquely up-regulated in the tamoxifen-resistant GEM models.

314HMGB1, IL-8 AND IL-8RA IN NON-INFECTIOUS ACUTE LUNG INJURY INDUCED BY WARM SALINE INFUSION IN RABBIT. Cilmery Suemi Kurokawa, Jose Roberto Fioretto, João Pessoa de Araujo Júnior, Rafaelle Batistella Pires, Susiane de Oliveira Klefens, Marcos Moraes, Rossano Cesar Bonatto, Maria Regina Moretto, Leonardo Teixeira Lopez, Mario Ferreira Carpi. Department of Pediatrics; Botucatu Medical School - Sao Paulo State University – UNESP.Immunologic and inflammatory aspects of severe acute lung lesion(ALI) or acute ARDS are not widely known. Previous studies have suggested involvement of HMGB1 and inflammatory cytokines, mainly IL-8,


as “deteriorating factor of lung lesion induced by ven-tilation”1,2. The aims of the study were to measure HMGB1, IL-8 and IL-8RA(receptor alpha of IL-8) levels in bronchoalveolar lavage (BAL) of rabbits with acute lung injury (ALI) induced by tracheal infu-sion of warm saline. Rabbits were anesthetized and tracheostomy tubes were inserted and connected in the mechanical ventilator Inter7. Lung lesion was induced by infusion and removal of warm saline in lung by tracheostomy tube3,4. The animals were assigned into two groups: 1) animals with no ALI; 2) animals with severe ALI. The groups were ventilated during 4 hours and HMGB1, IL-8 and IL-8RA were measured in BAL by the Elisa method. Lung injury induced by infusion of warm saline decreased pulmo-nary compliance (SG before: 1.86±0.576 > SG after: 0.67± 0,24) and oxygenation (PaO2 - SG before: 427.92 ± 89.90 > SG after: 68.18 ± 19.08). After a 4-hour period of ventilation the SG group had increased values of HMGB1, IL-8 and IL-8RA recep-tor. Conclusion: Increased levels of HMGB1, IL-8 and IL-8RA were detected in alveolar space after lung lesion induced by warm saline suggesting an associa-tion between HMGB1, IL-8 and IL-8RA levels and deterioration of lung. Fapesp: 2011/15144-21) Ogawa EM et al. Am J Respir Crit Care Med; 174:400-7; 2006. 2) Tadie JM et al. Am J Physiol Lung Cell Mol Physiol; 304:L342-9; 2013.3) Fioretto JR et al. Respir Care; 57:273-81; 2012. 4) Camporota L, Ranieri VM. Minerva Anestesiol; 78:1162-6; 2012.

315CR8 DEFICIENCY CAUSES EXACERBATION OF CONTACT HYPERSENSITIVITY DUE TO ENHANCED DENDRITIC CELL MIGRATION.Rikio Yabe, Kenji Shimizu, Soichiro Shimizu, Satoe Azechi, Byung-Il Choi, Sachiko Kubo, Shigeru Kakuta, Susumu Nakae and Yoichiro Iwakura, Tokyo University of Science, Noda, JapanChemokines recruit immune cells to targeted sites under physiological as well as inflammatory condi-tions. CCR8 is a chemokine receptor for CCL1 and CCL8, and regulates trafficking of immune cells including helper T cells, macrophages and monocytes. Although CCR8 has been implicated in the pathogen-esis of allergic contact dermatitis, the mechanism how CCR8 controls the skin diseases has not yet been elu-cidated. In the present study, we investigated the path-ological role of CCR8 in 2,4-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity (CHS), a murine model of allergic contact dermatitis. CCR8-deficient mice were more sensitive to DNFB-induced CHS compared with wild-type mice. This was corre-lated with increased numbers of granunocytes in the skin. In addition, T cell priming was aberrantly increased in draining lymph node from CCR8-deficient mice; T cell proliferation upon stimulation with an analog of DNFB, DNBS, was enhanced, and

interferon-g and interleukin-17 production were aug-mented. However, transfer of CCR8-deficient T cells did not exacerbate CHS response in recipient SCID mice, suggesting that CCR8 expression on T cells are dispensable for the pathogenesis of CHS. Notably, the accumulation of skin-resident dendritic cells (DCs) such as Langerhans cells and dermal DCs, and inflam-matory DCs in draining lymph nodes was highly enhanced in CCR8-deficient mice. Consistent with this observation, migration of cutaneous DCs from epidermis was remarkably elevated in CCR8-deficient mice in the sensitization process. These results sug-gest that CCR8 regulates DC migration from the skin to lymph nodes during the sensitization phase, and suppresses inflammatory responses in allergic contact dermatitis.

316EFFECTS OF POLLEN LIPIDS ON CYTOKINE SECRETION FROM PBMC IN ATOPIC AND NON-ATOPIC CASES. Mohammad Fereidouni and Shaghayeghsadat Nourani hassankiade, Asthma, Allergy & Immunology Research Center, Birjand University of Medical Sciences, Birjand, Iran.Pollens are the most important trigger of allergic symptoms in atopic patients. Pollen grains consist of several proteins which can act as allergens but they are also a rich source of different lipid components. These lipid materials are known for their physiologi-cal function in plant fertilization but may have also some role in immune response related to pollen. The aim of this study was to evaluate the effect of pollen lipid extract on secretion of IL-4 and IFN-γ from peripheral blood mononuclear cells (PBMCs) in pol-len sensitize and healthy cases. A mix lipid extract from five allergenic pollens were made by chloro-form/methanol method. PBMCs from 11 pollen sensi-tized patients and 8 healthy adults cultured for 48 hours with pollen lipid extract. Culture media, a mix aqueous pollen extract and PPD were used as con-trols. After 6 hours stimulation with phorbol ester (PMA) plus Ionomycin, IFNγ and IL-4 were mea-sured in supernatant by ELISA.In comparison to cul-ture media, aqueous pollen extract and PPD increased secretion of IFN-γ and IL-4 in both atopic and non atopic groups but the difference was not significant. Lipid extract significantly suppressed secretion of both cytokines in atopic and non atopic cases. The results of this study show that pollen lipid can sup-presses secretion of cytokines regardless to atopic state and suggest that pollen lipid may act as a potent modulator of immune responses.

317BH3 INTERACTING DOMAIN DEATH AGONIST GENE THERAPY ENHANCES ANTITUMOR EFFECT OF INTERFERON-ALPHA Takaya Tsuno(1), Shohei Kanno(1), Joseph Bekisz(2), Kathryn C. Zoon(2) and Noboru Tanigawa(1) ,(1)


Department of Radiology, Kansai Medical University, Osaka, Japan, (2) National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.Human interferon (IFN)-alpha has been approved for the treatment of certain types of cancer. Nevertheless, its effectiveness has met with varying degrees of suc-cess. To enhance the antiproliferative activity of IFN-alpha, in vitro and in vivo studies were performed. In initial IFN-alpha signaling, IFN regulatory factor (IRF) 9-RNA interference (RNAi) completely restored cell proliferation inhibited by IFN-alpha in human ovarian adenocarcinoma OVCAR3 cells sensitive to IFN-alpha. IRF9-RNAi followed by IFN-alpha treat-ment inhibited gene expression of tumor necrosis fac-tor-related apoptosis-inducing ligand (TRAIL) in OVCAR3 cells. Following TRAIL-mediated signal-ing, BH3 interacting domain death agonist (BID)-RNAi prevented IFN-alpha from collapsing mitochon-drial membrane potential. Plasmid pIRES-BID fol-lowed by IFN-alpha treatment significantly inhibited viability of human lung carcinoma A549 cells resis-tant to IFN-alpha. These results suggest that BID is crucial for cell viability regulated by IFN-alpha which can induce mitochondria-mediated apoptosis. The BID gene therapy was further assessed in a living body. Here, irradiation is known to be conventional cancer treatment and cause DNA damage. It is report-ed that DNA damage can collapse mitochondrial membrane potential. Accordingly, the effects of irradi-ation were also assessed because crosstalk with BID-induced mitochondrial apoptosis might exist. pIRES-BID and pegylated human IFN-alpha were intrave-nously and subcutaneously injected into nude mice bearing subcutaneous A549 xenografts, respectively. Irradiation was subsequently performed. Electron microscopy findings revealed mitochondrial apoptosis in A549 xenografts in pIRES-BID and IFN-alpha injected mice. Live imaging study detecting a fluores-cent tracer also indicated apoptosis induced by pIRES-BID and IFN-alpha in A549 xenografts. In the assessment of tumor volume, A549 xenografts in pIRES (mock) transfected mice kept growing after IFN-alpha injection or irradiation alone. On the other hand, IFN-alpha injection followed by irradiation remarkably inhibited tumor growth in pIRES-BID transfected mice. Consequently, the present study sug-gests that BID is a therapeutic candidate for targeted gene therapy of IFN-alpha resistant tumor.318PROTEIN KINASE C FAMILY AND Θ-SUBTYPE-SELECTIVE INHIBITORS R896 AND R682 BLOCK T CELL ACTIVATION AND PROTECT IN EXPERIMENTAL MODELS OF IMMUNE-MEDIATED DISEASE.S.J. Holland, M. Wang, M. Duncton, A. Owyang , E. Tai, S. Yi, S. Braselmann, A. Bagos , R. Roe, G. Park , C. Choy, R. Frances , S. Siu , C. Young, J. Zhang ,

H. Li , P. Pine, R. Singh, D.G. Payan, and E.S. Masuda, Rigel Inc., South San Francisco, CA, USA. Novel protein kinase C (PKC)-θ is a key signaling molecule in the T cell receptor (TCR) signaling path-way that is critical for T cell activation, proliferation and cytokine production, making it an attractive drug target for therapeutic intervention in autoimmune and inflammatory diseases. Using high-throughput screen-ing and optimization for inhibitors of TCR-induced IL-2 production in human primary T (huPriT) cells, we discovered a series of non-staurosporine small molecule compounds that selectively block PKCs. Lead compound R896 inhibited TCR signaling induced by anti-CD3/CD28 antibodies, staphylococcal enterotoxin B antigen (SEB) and the mixed leukocyte reaction (EC50 < 100nM), correlating with potent inhibition of PKC-θ in biochemical assays (IC50 < 2nM). R896 suppressed TCR-induced phosphoryla-tion of NFκB, Erk and p38 but not phosphorylation of the TCR-proximal adapter LAT or the PKC-θ activa-tion site, Thr538. R896 was inactive in a panel of tyrosine and serine-threonine kinase signaling assays in cells and was not cytotoxic. In a kinase panel, R896 inhibited only PKC family kinases > 50% at 250nM and exhibited moderate selectivity for PKC-θ over other PKC subtypes. In contrast, close analog R682 exhibited > 100x selectivity for PKC-θ over PKC-α /β in biochemical assays. In huPriT, R682 potently blocked IL2 production stimulated by anti-CD3/CD28 (EC50 ~65nM) and PMA/anti-CD28, which activates novel PKCs (EC50 38nM). However, R682 did not suppress IL2 stimulated by PMA/ionomycin, which activate both novel and conventional PKCs (EC50 2.4µM), confirming that pronounced PKC-θ selectivi-ty is maintained in cells. Interestingly, both com-pounds exhibited similar on-target efficacy when administered orally in vivo, in acute, SEB-induced IL2, and chronic T cell-dependent inflammatory dis-ease models, highlighting the central role of PKC-θ in these models. Availability of both PKC family and highly θ-subtype-selective oral PKC inhibitors facili-tates further interrogation of the role of the PKC fami-ly in disease.

319DEVELOPMENT OF SANDWICH IMMUNOASSAYS FOR QUANTIFICATION OF TOTAL TGFß1, FREE ACTIVE TGFß1, LATENCY-ASSOCIATED PEPTIDE (LAP) AND LATENT TGFß IN BIOLOGICAL SAMPLESLingpu Dong, Takatoku Oida, Jie Zhou, Binggang Sun, Jianyong Huang, Naomi Urbina, and Shaoquan Ji , BioLegend, Inc., San Diego, CA 92121.TGF ß controls cell proliferation and differentiation and many other biological processes. As a circulating protein, TGFß1 exists, to far less extent, in a free/ active/ homodimeric form that plays direct biological roles, and predominantly in a complex form with


latency-associated peptide (LAP) forming small latent TGFß , and subsequently with latent TGF-beta bind-ing protein (LTBP) forming large latent TGFß, which further interacts with other proteins in circulation . The complex nature of the system makes it difficult to understand exact roles of each component in biologi-cal processes without availability of proper analytical methods to quantify these components individually. Present studies describes development of individual immunoassay methods to quantify total TGFß1, free active TGFß1, latency-associated peptides (LAP), and latent TGFß. The antibodies and recombinant protein standards used in the assays were developed and man-ufactured at BioLegend, Inc. The sandwich assays were analytically and biologically validated to ensure that assay methods are specific, sensitive, accurate, reproducible and robust. The assays were tested for cell culture supernatant, serum and plasma samples. Free active TGFß1 assays allows detection of low pg/mL concentrations in biological sample, which were not possible previously. Assays for LAP and latent TGFß provide novel tools to study LAP and latent TGFß in regulation of TGFß1 activity and their direct biological functions. Commercial availability of these assay products enables consistent supply of quality assays for biomedical studies.

320CYTOKINES AND CELLULAR RESPONSES TO NIPAH VIRUS-LIKE PARTICLESPramila Walpita, Gary Klimpel, and Janice Endsley, University of Hawaii School of Medicine, Honolulu, Hawaii USAWe have shown previously that vaccination of mice with (NiV)-like particles (VLPs) composed of NiV G, F and M proteins results in the induction neutralizing antibody response, a key correlate of vaccine efficacy. As a part of our studies to understand the mechanisms of induction of adaptive response by NiV VLPs, we have tested the physical interaction of these particles with human immature dendritic cells (iDCs), the key antigen presenting cells that serve as a link between innate and adaptive immune response. We have stud-ied the phenotypic and functional consequences to this interaction. Our results show iDCs were able to bind NiV VLPs and internalize them. Analysis by flow cytometry and enzyme immunoassays showed that this interaction resulted in the maturation and activation of the iDC including up-regulation of co-stimulatory molecules, and the induction of proin-flammatory cytokines.

321DECTIN-1 SIGNALING SYNERGISTICALLY ENHANCES TOLL-LIKE RECEPTOR-MEDIATED PRODUCTION OF INTERFERON BETA Motohiko Kadoki, Yamato Sasaki, Ce Tang, Tomonori

Kamiya and Yoichiro Iwakura , Division of Experimental Animal Immunology, Research Institute of Biomedical Sciences, Tokyo University of Science, Noda, Chiba, Japan.

Innate immune receptors such as Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) sense pathogen- or danger-associated molecular patterns. Detection of such molecules by dendritic cells directs acquired immunity to appropriate responses. Dectin-1, one of CLRs, is the receptor for β-glucans, which are produced by several bacteria, fungi or seaweeds. We previously generated Dectin-1-deficient mice and reported that Dectin-1 was essential for host defense against fungal infection. Dectin-1 engagement by itself activates several signal transduction pathways and leads to the production of cytokines and reactive oxygen species. In addition, Dectin-1 signal synergis-tically enhances the production of proinflammatory cytokines such as TNF and IL-12 induced by Toll-like receptor (TLR) stimulation. In this study, we exam-ined the role of Dectin-1 signaling on the production of type I interferon (IFN) and demonstrated that IFN-β production from bone marrow-derived dendrit-ic cells (BMDC) was regulated by Dectin-1-mediated signal. We found that BMDC produced IFN-β by the stimulation with curdlan, a bacteria-derived β-glucan, in a Dectin-1-dependent manner. On the other hand, depleted-zymosan, a fungus-derived highly pure β-glucans, did not induce IFN-β production. Thus, we next examined possible effect of contaminated LPS in the curdlan preparation in curdlan-mediated IFN-β production, and found that inhibition of LPS activity by polymyxin B reduced IFN- β production. Consistent with this, co-stimulation with LPS and depleted-zymosan synergistically enhanced IFN-β production from BMDC, although depleted-zymosan alone did not induce IFN-β. Dectin-1 signal synergis-tically enhanced IRF3 activation in the presence of LPS but Dectin-1 signal by itself did not activated IRF3. Furthermore, mitogen-activated protein kinases such as ERK, JNK, and p38 were additively activated by co-stimulation of TLR4 and Dectin-1. Those acti-vations augmented IFN-β production at the transcrip-tion level especially in the late phase, resulting in pro-longed activation of IFN-β transcription. Dectin-1 sig-nal also enhanced TLR9-mediated IFN-β production. These results indicate that Dectin-1 cooperate with TLRs to produce type I IFN as well as proinflamma-tory cytokines efficiently. Furthermore, it suggested that combinatorial vaccination with TLR ligands and β-glucans would be more effective than TLR ligands alone to induce IFNs.

322The N-Terminus of Unc93b is Cleaved by Host and Enteroviral ProteasesKatharine G Harris and Carolyn Coyne, University of Pittsburgh Medical School, Pennsylvania


Coxsackievirus B3 (CVB3) is a non-enveloped, posi-tive-sense ssRNA virus belonging to the enterovirus genus. CVB infections are associated with a number of diverse syndromes, including meningitis, pericardi-tis, febrile illness, diabetes, and are commonly associ-ated with dilated cardiomyopathy and myocarditis. Studies in vivo have pointed to a prominent role for toll-like receptor (TLR3) in the control of CVB3-induced disease. Unc93b is an endoplasmic reticulum (ER)-resident transmembrane protein that serves to traffic TLR3, and other endosomal TLRs, from the ER to the endosome and therefore is indispensible for TLR3 signaling. Here, we show that CVB3 utilizes the virally-encoded protease 3Cpro to cleave Unc93b at a specific residue within its N-terminus (residue Q17). In addition, we find that the N-terminus of Unc93b is also subjected to caspase-mediated cleav-age at position D27 during apoptotic cell death. Interestingly, both 3Cpro- and caspase-mediated cleav-age of Unc93B removes only a small portion of the N-terminus and does not alter the association of the C-terminal fragment with the ER. Collectively, our results suggest that the targeting of Unc93b by both host and enteroviral proteases within a small (~10 amino acid) region may suggest an important and pre-viously uncharacterized role for this region in the function of Unc93b. We are currently investigating the role of these cleavage events in TLR and cell death signaling.

323CHEMICAL GENETICS REVEAL THAT JANUS KINASE 3 CATALYTIC ACTIVITY IS REQUIRED FOR INTERLEUKIN-2 SIGNAL TRANSDUCTIONGeoffrey A. Smith1, Arthur Weiss2,3, and Jack Taunton2,4, 1Chemistry and Chemical Biology Graduate Program, 2Howard Hughes Medical Institute, 3Division of Rheumatology, Department of Medicine, Rosalind Russell Medical Research Center for Arthritis and 4Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, USA.The common γ-chain cytokines, including Interluekin-2 (IL-2), are thought to require both Janus Kinase 1 (Jak1) and Janus Kinase 3 (Jak3) activity for signal transduction. A recent study by Haan et al. has challenged this model (1). These authors used phar-macological and chemical genetic approaches to eval-uate the relative contributions of Jak1 and Jak3 kinase activity to IL-2 signaling. Their results suggested that, whereas Jak1 kinase activity is essential for IL-2 sig-naling, Jak3 activity is not. To further explore the notion that Jak3 only plays a scaffolding function, we developed a series of Jak3 inhibitors that target a cysteine (Cys909) found in Jak3 but not in other Jak-family kinases. The resulting compounds have single-digit nanomolar potency against IL-2 driven prolifera-

tion of primary murine CD4+ cells, and greater than 100-fold selectivity over Jak3-independent cytokine signaling. Furthermore, retroviral overexpression of a drug-resistant Jak3 mutant (C909S) substantially res-cues this effect, suggesting that these compounds act in a Jak3-dependent manner. Based on these studies, we conclude that blocking Jak3 catalytic activity is sufficient to inhibit IL-2 induced proliferation of T cells. Further studies are ongoing to understand the respective roles of Jak1 and Jak3 activity in proximal IL-2 signaling events, including STAT5 phosphoryla-tion. Support List](1) Haan, C., et al (2011). Jak1 Has a Dominant Role over Jak3 in Signal Transduction through γc-Containing Cytokine Receptors. Chem Biol 18, 314–323.

324DISTINCT ROLES OF IL-25 AND IL-33 IN SPONTANEOUS ARTHRITIS IN INTERLEUKIN-1 RECEPTOR ANTAGONIST-DEFICIENT MICE.Aya Nambu(1), Katsuko Sudo(2) and Susumu Nakae(1). (1) Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, Japan, (2) Animal Research Center, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.Rheumatoid arthritis (RA) is an autoimmune disease characterized by progressive joint inflammation and destruction of cartilage and bone. The deficiency of IL-1 receptor antagonist (IL-1Ra) in mice resulted in the spontaneous arthritis due to excessive IL-1 signal-ing. IL-17 and TNF are known to be responsible for the development of spontaneous arthritis in IL-1Ra-/- mice. Both IL-25 and IL-33 can induce Th2 cytokines by various types of cells such as Th2 cells, NKT cells and ILC2, contributing to the host defense against nematodes and the development of allergic disorders. It was shown that IL-25 could suppress, but IL-33 could enhance, the development of Th17 cell-mediat-ed autoimmune diseases such as experimental autoim-mune encephalomyelitis or collagen-induced arthritis in mice suggesting that IL-25 and/or IL-33 also may contribute to the development of IL-17-mediated spontaneous arthritis in IL-1Ra-/- mice. To elucidate this, we generated IL-25-/- IL-1Ra-/- mice and IL-33-/- IL-1Ra-/- mice, and found that IL-33 rather than IL-25 was important for the development of spontaneous arthritis in IL-1Ra-/- mice.

325PROTEASOME DEFECTS IN CANDLE PATIENTS’ CELLS LEAD TO IFN PRODUCTION IN BOTH HEMOPOIETIC AND NON-HEMOPOIETIC CELLS. Yin Liu1, Angelique Biancotto2, Yan Huang1, Massimo Gadina, John Philip McCoy2, Raphaela Goldbach-Mansky1.1Translational Autoinflammatory


Disease Section, NIAMS, NIH, Bethesda, MD. 2Center for Human Immunology, NHLBI, NIH, Bethesda, MD. 3Office of Science and Technology, NIAMS, NIH, Bethesda, MD.CANDLE (Chronic Atypical Neutrophilic Dermatosis with Lipodystrophy and Elevated Temperature) syn-drome is an autoinflammatory disease caused by auto-somal recessive mutations in PSMB8 and other sub-units of the proteasome. CANDLE patients’ whole blood microarray analysis showed that many IFN reg-ulated genes were strongly upregulated and mono-cytes from CANDLE patients showed STAT1 hyper-activation in response to IFN-γ stimulation. We hypothesized that cellular stress caused by the protea-some defects in CANDLE patients leads to IFN pro-duction and asked whether the IFN production and response is restricted to certain hematopoietic cells or present in non-hematopoietic cells as well. We studied IFN-α and IFN-γ production in PBMCs and fibro-blasts from CANDLE patients or in healthy cells treated with proteasome inhibitor epoxomicin. Using intracellular staining and flow cytometer analysis, we found increased production of IFN-α and IFN-γ in NK, T and dendritic cells from the two CANDLE patients tested compared with healthy controls. Increased IFN production could be reproduced in PBMCs from healthy individuals that were treated with epoxomicin. The increase in protein staining for IFNs was paralleled by increased of message mea-sured by qPCR. To study IFN production in non-hemopoietic cells, we used fibroblasts and observed increased IFN-α message in CANDLE patients’ fibro-blasts compared to healthy controls. Similar to PBMCs, epoxomicin treated healthy fibroblasts also increased IFN-α message. Interestingly message for other inflammatory cytokines, including TNF-α, IL-1 and IL-6, were either not change or even suppressed. Consistent with increased IFN production in CANDLE patient cells, microarray study showed that IFN regulated genes were upregulated in sorted T, B, NK cells, monocytes and neutrophils. CANDLE patients’ leukocytes also showed upregulated MHC I expression, suggesting increased IFN signaling in those cells. We conclude that proteasome defect causes IFN production in both hemopoietic and non-hemopoietic cells in CANDLE patients that can lead to increased IFN signaling.

326TOXOPLASMA GONDII-INDUCED TH1 CELLS AND INTESTINAL DYSBIOSIS COOPERATE IN IFN-G-DEPENDENT ELIMINATION OF PANETH CELLSMegan Raetz1, Sun-hee Hwang1, Cara Wilhelm1, Carolyn Sturge1, Julie Mirpuri1, Lora V Hooper1,2 and Felix Yarovinsky1, 1Department of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. 2The Howard Hughes Medical

Institute. Activation of Toll-like receptors (TLRs) by pathogens triggers cytokine production and T cell activation, immune defense mechanisms that are linked to immu-nopathology. Here we show that IFN-g production by CD4+ Th1 cells during mucosal responses to the pro-tozoan parasite Toxoplasma gondii resulted in dysbio-sis and the elimination of Paneth cells. Paneth cell death led to loss of antimicrobial peptides and occurred in conjunction with uncontrolled expansion of the Enterobacteriaceae family of Gram-negative bacteria. The expanded intestinal bacteria were required for the parasite-induced intestinal pathology. The investigation of cell type–specific factors regulat-ing Th1 polarization during T. gondii infection identi-fied the T cell–intrinsic TLR pathway as a major reg-ulator of IFN-g production in CD4+ T cells responsi-ble for Paneth cell death, dysbiosis and intestinal immunopathology.

327MAMMARY-SPECIFIC GENE ACTIVATION IS DEFINED BY PROGRESSIVE RECRUITMENT OF STAT5 DURING PREGNANCY AND THE ESTABLISHMENT OF H3K4ME3 MARKSKeunsoo Kang, Daisuke Yamaji, Gertraud W. Robinson, Lothar Hennighausen, National Institutes of Health,Bethesda, Maryland Differentiation of mammary secretory epithelium dur-ing pregnancy is characterized by sequential activa-tion of genes over several orders of magnitude. While some of these genes are already expressed in imma-ture alveolar cells, others are activated only with the completion of differentiation. Although the transcrip-tion factor STAT5 is key to alveolar development, it is not clear to what extent it controls the temporal acti-vation of genetic programs in secretory epithelium. To uncover molecular mechanisms supporting progres-sive gene activation, we explored genome-wide STAT5 binding and H3K4me3 marks in undifferenti-ated and differentiated mammary tissues at early preg-nancy and parturition, respectively. STAT5 binding to genes specifically induced during pregnancy was lim-ited in immature mammary tissue but increased sharp-ly in fully differentiated epithelium. This increase was associated with the establishment of H3K4me3 marks and transcriptional activation. In contrast, STAT5 tar-get genes that are expressed in a variety of cell types were equally recognized by STAT5 in immature and mature tissues. Most notably, STAT5 binding preced-ed the formation of H3K4me3 marks in mammary specific genes. In addition, we established an exhaus-tive mammary transcriptome and discovered novel mammary-specific alternative promoters and genes including non-coding RNAs. Our findings suggest that STAT5 is an early step in establishing transcrip-tion complexes on cell-specific genes. This is the first


study in an organ that links progressive chromatin occupancy of STAT5 to the acquisition of H3K4me3 and transcription during differentiation.

328DIAGNOSTIC UTILITY OF COPEPTIN IN ADDITION TO HIGH-SENSITIVITY CARDIAC TROPONIN FOR THE EARLY DIAGNOSIS OF NON-ST-ELEVATION ACUTE CORONARY SYNDROME.Elena Toniato, Rosa Di Scala, Ivana Cataldo, Fabrizio Ricci, Doranna De Pace, Raffaele De Caterina , University of Chieti, Chieti, ItalyAims. Rapid and reliable exclusion of acute myocardial infarction (AMI) during an emergency department (ED) triage is a major unmet clinical need. We aimed at verifying the non-inferiority of a single-sampling strategy of hs-cTn and copeptin compared with the dual hs-cTn sampling for the early diagnosis of Non-ST-Elevation Acute Coronary Syndromes (NSTE-ACS) versus Non-Coronary Chest Pain (NCCP) in a selected cohort of consecutive patients admitted at the Emergency Department.

329MECHANISMS OF AUTOINHIBITION AND INFLAMMASOME ASSEMBLY REVEALED BY THE STRUCTURE OF THE AIM2 PYRIN DOMAINTengchuan Jin, Andrew Perry, Patrick Smith, Jiansheng Jiang, and T. Sam Xiao, Structural Immunobiology Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA 20892-0430.AIM2 is a cytosolic dsDNA sensor essential for innate immune responses against DNA viruses and bacteria such as Francisella and Listeria. Upon dsDNA engagement, the AIM2 amino terminal pyrin domain (PYD) is responsible for downstream signaling to the adapter protein ASC through homotypic PYD:PYD interactions and the assembly of an inflammasome. Towards a better understanding of the AIM2 signaling mechanism, we determined the crystal structure of the human AIM2 PYD. The structure reveals a death domain fold, with a short a3 helix that is buttressed by a highly conserved lysine residue at the a2 helix, which may stabilize the a3 helix for potential interaction with partner domains. The surface of the AIM2 PYD exhibits distinct charge distribution, with highly acidic a1-2 helices and highly basic a5-6 helices. A prominent solvent-exposed hydrophobic patch formed by residues F27 and F28 at the a2 helix resembles a similar surface involved in the death effector domain homotypic interactions. Docking studies suggest that the AIM2 PYD may bind the AIM2 HIN domain or ASC PYD using overlapping surface near the a2 helix. This may ensure that AIM2 interacts with the downstream adapter ASC only upon release of the autoinhibition by the dsDNA ligand. Our work thus unveils novel structural features of the AIM2 PYD, and provides insights into the potential mechanisms of the PYD:HIN and PYD:PYD interactions

important for the AIM2 autoinhibition and inflammasome assembly.

330TNF-SUPERFAMILY MEMBER TL1A ELICITS TYPE 2 INNATE LYMPHOID CELLS AT MUCOSAL BARRIERS.Xin Yu, Rajita Pappu, Vladimir Ramirez-Carrozzi, Patrick Caplazi, Juan Zhang, Donghong Yan, Min Xu, Wyne P. Lee, and Jane L. Grogan, Genentech, South San Francisco, California USAImmune responses at mucosal barriers are regulated by innate Type 2 lymphoid cells (ILC2) that elaborate effector cytokines IL5 and IL13. IL25 and IL33 are key cytokines that support ILC2s, however, mice deficient in these pathways retain some functional ILC2s. Analysis of human and murine cells revealed that ILC2s highly express TNF-receptor superfamily member DR3 (TNFRSF25). Engagement of DR3 with cognate ligand TL1A promoted ILC2 expansion, survival and function. Exogenous protein or genetic overexpression of TL1A activated ILC2 cells independent of IL25 or IL33. Dr3-/- mice failed to control gut helminthic infections, and failed to mount ILC2 responses in the lung after nasal challenge with papain. Our data demonstrates a key role for TL1A in promoting ILC2s at mucosal barriers.

331WOUND HEALING EFFECTS AND POSSIBLE MECHANISM OF ACTION OF THE BUTANOL FRACTION FROM HYDNOCARPI SEMEN CRUDE EXTRACT IN VITRO ACUTE INFLAMMATION MODEL.Geum Seon Lee 1,3, Ki Man Lee1,3, Hong Shim1,3, Seung Hyun Kim 1,3, Dong Sool Yim1, Jae Hoon Cheong 1,2 and Tae Jin Kang 1,3*, 1College of Pharmacy, Sahmyook University, Seoul, 139-742 Korea, 2 Uimyung Research Institute for Neuroscience, Sahmyook University, Seoul, 139-742 Korea, 3 Institute of Chronic Disease, Sahmyook University, Seoul, 139-742 Korea.In previous study showed that fractions of n-Hexane, ethylacetate (EtOAc), and butanol (BuOH) from HS crude extract were evaluated for their wound healing activity by using in vivo ulcer models. Although n-Hexane and EtOAc fractions promote wound heal-ing in mice with ulcer, the BuOH fraction exhibited the most potent wound healing activity and the wound area score significantly decreased after treatment of BuOH fraction. In present study, BuOH fraction from HS crude extract was evaluated for their wound heal-ing effect by using in vitro acute inflammation model. The BuOH fraction stimulated peritoneal cells and RAW264.7 cell to increase the production of nitric oxide (NO), IL-6, IL-10, VEGF and TNF-a. The frac-tion inhibited the LPS-induced production of NO, VEGF, and TGF-β at a dose-dependent manner. It also


activated mouse keratinocyte to increase the produc-tion of IL-6 and TNF-a. The mRNA expression and activation of IL-1β and TLR2 were increased by BuOH fraction, while LPS-induced IL-1β and TLR2 expression were decreased. The mechanism that the HS helps to promote healing by inflammation is pos-sibly associated with the production of TNF-a as well as the secretion of VEGF, IL-6, IL-10 and TLR2, which were involved to mediate innate immune responses to a variety of stimuli. Keyword s; Hydnocarpi Semen, butanol fraction, inflammation, Cytokines.

332MATERNAL AND FETAL T CELL RESPONSES DURING NORMAL PREGNANCY AND PRETERM LABOR. Michela Frascoli1, 2, Lacy Coniglio1, 2, Qizhi Tang2, Tippi C. MacKenzie1,2, 1Eli and Edy the Broad Center of Regeneration Medicine, 2Department of Surgery, UCSF, San Francisco, California, USA.Pregnancy is the most successful form of graft toler-ance, involving multiple mechanisms that protect the semi-allogeneic fetus from attack by the maternal immune system. We have previously shown that murine maternal T cells are crucial players in the onset of preterm labor in mice and hypothesized that pregnancy complications in humans may also corre-late with increased maternal T cell reactivity against the fetus. We first isolated peripheral blood mononu-clear cells (PBMCs) from maternal and cord blood during normal pregnancy, pregnancy complications such as preterm labor, and blood from not pregnant women as controls. To analyze direct maternal T cell reactivity against fetal antigens, we performed mixed lymphocyte reactions between CFSE-labeled maternal responder cells and fetal stimulated B cells, which we culture to serve as antigen presenting cells (APCs). We also analyzed indirectly-reactive T cells (which have been shown to be more relevant in pregnancy) by culturing maternal PMBCs with maternal sBc and fetal cell lysate. We observed significantly lower per-centages of directly-reactive CD4+ T cells in pregnant women compared to non-pregnant controls. However, PBMCs of pregnant women show a robust prolifera-tion when stimulated with a-CD3 and a-CD28 anti-bodies, indicating that these T cells are not unable to proliferate in response to TCR triggering. Interestingly, the percentage of proliferating fetal T cells against maternal APCs was significantly higher than that of maternal T cells with fetal APCs. Most importantly, in pregnancies complicated with preterm labor, there are significantly more maternal CD4 T cells that react against the fetal antigens through the indirect pathway compared to normal pregnancies. Determining whether pregnancy complications involve maternal anti-fetal T cell responses has clini-cal implications for the treatment of diseases such as preterm labor.

333TNF-Superfamily Member TL1A Elicits Type 2 Innate Lymphoid Cells at Mucosal BarriersXin Yu1, Rajita Pappu1, Vladimir Ramirez-Carrozzi1, Patrick Caplazi2, Juan Zhang3, Donghong Yan3, Min Xu3, Wyne P. Lee3, Jane L. Grogan1*, Departments of 1Immunology, 2Pathology and 3Translational Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080Immune responses at mucosal barriers are regulated by innate Type 2 lymphoid cells (ILC2) that elaborate effector cytokines IL5 and IL13. IL25 and IL33 are key cytokines that support ILC2 differentiation and function. Interestingly, while mice deficient for IL25 or IL33 or the receptors for IL25 or IL33 have impaired ILC2 responses, some functional ILC2 cells still remain, indicating the existence of additional pathways that support ILC2 biology. Consequently, we determined whether other pathways are necessary for eliciting ILC2 responses. Analysis of human ILC2s by microarray revealed that the TNF receptor superfamily (TNFRSF) member DR3 (TNFRSF25) was highly expressed on human ILC2s, which we confirmed on murine ILC2s. Engagement of DR3 with cognate ligand TL1A (TNFSF15) promoted ILC2 expansion, survival and function. TL1A is expressed primarily by activated myeloid cells and stressed epi-thelial cells, including gut mucosa. Exogenous protein or genetic overexpression of TL1A activated ILC2 cells independent of IL25 or IL33. Dr3-/- mice failed to control gut helminthic infections, and failed to mount ILC2 responses in the lung after nasal chal-lenge with papain. Our data demonstrates a key role for TL1A in promoting ILC2 cell proliferation and activation at mucosal barriers.

334ANTIGEN-SPECIFIC TOLERANCE REQUIRING REGULATORY T CELLS. Craig P. Chappell(1)*, Natalia V. Giltiay(1)*, Kevin E. Draves(1), Kevin Chen(1), Mark J Shlomchik(2), Daniel H. Kaplan(3), and Edward A. Clark(1) (1)

Department of Immunology, University of Washington, Seattle, Washington, USA, (2) Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA and (3) Department of Dermatology, University of Minnesota, Minneapolis, Minnesota, USA * Equal contribution Plasmacytoid dendritic cells (pDCs) were originally called natural interferon (IFN)-producing cells due to their ability to secrete large amounts of type I IFNs after stimulation by TLR7 or TLR9 agonists such as viral RNAs and DNAs. Patients with systemic lupus erythematosus (SLE) have dysregulated pDCs and increased expression of IFN regulated genes. The C-type lectin receptor BDCA2 (Blood Dendritic Cell Antigen 2) is expressed exclusively on human pDCs and signaling through BDCA2 can block the ability of


pDCs to produce type I IFNs in response to TLR ligands, and also has been shown to play a role in Ag capturing, internalization and presentation to T cells. With a goal of testing whether BDCA2 could be used to regulate pDCs and IFN in vivo, we established transgenic mice expressing the human BDCA2 just in pDCs and backcrossed to C57BL/6 mice (B6.BDCA2 Tg mice). We delivered Ags directly to pDCs using anti-BDCA2 mAbs to which Ags had been attached, and studied the effect of delivering Ags to pDCs on T and B cell responses. Delivery of the protein OVA to pDCs through BDCA2 (OVA-aBDCA2) resulted in a significant reduction in the numbers of OVA-specific effector T cells but increased the percentage of OVA-specific Foxp3+ regulatory T cells (Tregs). Upon rechallenge with OVA in adjuvant (alum), mice previ-ously treated with only 1 mg OVA-aBDCA2, unlike controls, had a dramatic reduction in OVA-specific IgG Ab production. This OVA-aBDCA2-induced Ag specific tolerance could be reversed by treating toler-ized mice with anti-CD25 to reduce Treg cell levels prior to rechallenge with OVA/Alum. Targeting Ags to BDCA2+ pDCs may be a useful approach for treat-ment of autoimmune diseases, which involve activa-tion of pathogenic Ag-specific T-cells and Ab produc-tion. (supported by NIH grant AI52203)

335SOLUBLE TYPE I INTERFERON RECEPTOR IS ELEVATED BY INTERFERON TREATMENT AND IN CERTAIN AUTOIMMUNE DISEASESTaher Fatakdawala1, Michael Skawinksi1, Jonathan Ferriera2, Tara Stauffer1, Thomas B. Lavoie1, 1Product Research & Development and Assay Services, PBL Assay Science, Piscataway, New Jersey, USA. 2Quality Control, PBL Assay Science, Piscataway, New Jersey, USA.The Type I Interferon (IFN) receptor is a heterodimer of chain 1 (IFNAR1) which is required for signaling, and chain 2 (IFNAR2) which binds tightly to IFN. Soluble forms of IFNAR2 can be produced by prote-olytic cleavage or production of an alternatively spliced transcript. Soluble IFNAR2 can be found in serum and urine however its role and regulation are poorly understood. Studies have suggested that sIF-NAR2 may be elevated in MS patients, advanced can-cer patients and hepatitis C infected patients. Using a newly developed ELISA for sIFNAR2 we have exam-ined commercially sourced serum/plasma samples from autoimmune patients and normal healthy donors. The average sIFNAR2 levels are 2.6±0.7 ng/ml with no difference observed between male (n=30) and female donors (n=30). MS patients on IFN therapy (n=29) had significantly (p=0.0002) increased levels of sIFNAR2 than normal donors, Those on other ther-apies (n=24) were not different from the normal popu-lation but were significantly different than the MS patients on IFN therapy (p=0.0001). IFN-Beta was

measurable in 86% of those patients treated with IFN. IP-10 levels in these patients correlated with IFN dose (r=0.747) while sIFNAR2 did not. sIFNAR2 levels showed no correlation with treatments such as vita-min-D, copaxone or natalizumab. Systemic Lupus patients (n=67) had elevated sIFNAR2 (p=<0.0001) while rheumatoid arthritis (n=16) were not signifi-cantly different from normal. Nor were Sjogren’s patients (n=11) and scleroderma pateints (n=10). Although evidence of Type I IFN activation has been observed in RA, Sjogren’s and Scleroderma patients the intensity is thought to be less than that observed for MS patients on IFN-therapy and Systemic Lupus. These data are consistent with a model where long term IFN signaling above a certain threshold leads to elevated sIFNAR2.

ABSTRACTS OF INVITED SPEAKER TALKS

S-8Regulation of Barrier ImmunityDavid ArtisPerelman School of Medicine, University of Pennsylvania, Philadelphia, USAEmploying diverse models of microbial colonization, pathogen infection and chronic inflammation, research in the Artis lab is examining how mammalian host genetics and signals derived from commensal micro-bial communities influence innate and adaptive immune responses in the skin, lung and intestine. Epithelial cells (ECs) were recently shown to play a critical role in maintaining the balance of tolerance, immunity and inflammation at barrier surfaces includ-ing the gastrointestinal tract. We are employing induc-ible deletion or overexpression of genes in intestinal ECs to interrogate how they regulate the functions of intestinal myeloid and lymphocyte lineages. The long-term goals of these studies are to improve oral vacci-nation against enteric infections and prevent chronic inflammation associated with diseases including food allergy and inflammatory bowel disease. We are are employing gnotobiotic mice to examine the influence of commensal microbial communities on intestinal and peripheral immune cell development and func-tion. Our findings indicate that commensal microbes have a major regulatory influence on CD4+ T cell and granulocyte function associated with susceptibility to multiple inflammatory diseases. In related studies, we are investigating how ECs regulate allergen- or helm-inth-induced type 2 inflammation at mucosal sites. Secretion of IEC-derived cytokines including IL-25, IL-33 and thymic stromal lymphopoietin (TSLP) appear to be important early events in influencing dendritic cell and CD4+ T cell responses required these responses. Our recent studies suggest that ECs also govern extramedullary hematopoiesis that can influence the development of TH2 cytokine responses. It is hoped that the results of these studies will


advance understanding the pathophysiology of multi-ple mucosal inflammatory diseases, including asthma, allergy and inflammatory bowel disease and provide a framework to test the therapeutic potential of manipu-lating epithelial cell responses in these disease states.

S-9The Role of Cytokines in Infection and InflammationEddy F Y LiewInstitute of Immunology, Infection and Inflammation, University of Glasgow, United KingdomCytokines are hormones of the immune system. Cytokine-targeting represents a major triumph in immunology scientifically, clinically and commercial-ly. There is therefore considerable interest in discover-ing novel cytokines. I will illustrate the pleiotropic role of some of the novel cytokines by focusing on interleukin (IL)-33. IL-33 is the latest member of the IL-1 family. It is the ligand of ST2, which is expressed mainly on activated Th2 cells, epithelial cells, neuronal cells and mast cells. IL-33 can skew a predominantly Th1 cell population to Th2 cells phe-notype in vivo. Furthermore IL-33 potently induces alternatively activated macrophages (M2). IL-33 sig-nals via MyD88, the canonical pathway shared by all members of the IL-1 family. Additionally, IL-33 acti-vates type II cytokines via mTOR (mammalian target of rapamycin). IL-33 mRNA is expressed early during infection of the intestinal-dwelling nematode Trichuris muris in mice and IL-33 treatment enhances resis-tance to Trichuris infection by inducing Th2. Furthermore, IL-33 reduces the pathology and mortal-ity of experimental cerebral Malaria infection in mice by activating M2. Importantly, IL-33 also effectively attenuates sepsis by mobilising the innate cells neutro-phils, to the site of infection and helps to clear the pathogens. Thus IL-33 is evolutionally preserved for the host defence against infections. However, IL-33 can also induce Type 2 innate lymphoid cells (ILC2), which mediate airway inflammation. Furthermore, IL-33 contributes to the severity of mucocytis accom-panying chemotherapy (Irinatecan). Blocking IL-33 prolongs the treatment and effectiveness of chemo-therapy in colorectal cancer. In contrast, IL-33 appears to restore the long-term potentiation in a murine model of Alzheimer’s disease. Therefore, IL-33 is a double-edged sword and targeting IL-33 should be approached with caution.

S-10Non-Canonical Inflammasome Activation TargetsCaspase-11Vishva M. DixitGenentech, Inc., South San Francisco, California USACaspase-1 activation by inflammasome scaffolds com-prised of intracellular nucleotide-binding oligomeriza-tion domain (NOD)-like receptors (NLR) and the

adaptor ASC is believed essential for production of the pro-inflammatory cytokines interleukin (IL)-ß and IL-18 during the innate immune response. Here we show with C57BL/6 gene-targeted mice that cas-pase-11 (also known as caspase-4) is critical for cas-pase-1 activation and IL-1ß production in macrophag-es infected with Escherichia coli, Citrobacter rodenti-um, or Vibrio cholerae. Mouse strain 129 exhibited similar defects in IL-1ß production and harboured a mutation in the Casp11 locus that attenuated cas-pase-11 expression. This finding is important because published targeting of the Casp1 gene was done using 129 ES cells. Casp1 and Casp11 are too close in the genome to be segregated by recombination so the published Casp1–/– mice lack both caspase-11 and caspase-1. Interestingly, Casp11–/– macrophages secreted IL-1ß normally in response to ATP and monosodium urate, suggesting that caspase-11 is engaged by a non-canonical inflammasome. Casp1–/–

Casp11129mt/129mt macrophages expressing caspase-11 from a C57BL/6 BAC transgene failed to secrete IL-1β regardless of stimulus, confirming an essential role for caspase-1 in IL-1ß production. Caspase-11 rather than caspase-1, however, was required for non-canonical inflammasome-triggered macrophage cell death, indicating that caspase-11 orchestrates both caspase-1-dependent and -independent out-puts. Caspase-1 activation by non-canonical stimuli required NLRP3 and ASC, but caspase-11 processing and cell death did not, suggesting a distinct activator of caspase-11. Finally, loss of caspase-11 rather than caspase-1 protected mice from a lethal dose of lipopolysaccharide (LPS). These data highlight a unique proinflammatory role for caspase-11 in the innate immune response to clinically significant bac-terial infections.

S-11Classical and Non-Classical Cytokines in the Regulation of Innate ImmunityTadatsugu TaniguchiThe University of Tokyo, JapanClassical cytokines such as interferons (IFNs) and interleukins are those that are secreted by and signal to cells following innate immune receptor stimulation to regulate immune system activation. Recent advanc-es have resulted in a strong appreciation for the role of what we term non-classical cytokines, released by cell death or unknown secretion mechanisms(s) to also regulate the immune system. This class of cytok-ines is perhaps best represented by the high-mobility group box 1 (HMGB1) protein, which serves multiple functions in the regulation of inflammation. For instance, HMGB1 acts as a ligand that can evoke inflammatory responses, and as a sensor for triggering nucleic acid-mediated immune responses. I will pres-ent recent data obtained using HMGB1 conditional knockout mice that indicate its protective and patho-


logical functions to the host. Finally, I will also shift topics to describe how members of the IRF family of transcription factors, which we originally discovered in the context of type I IFN responses, participate in “beneficial signal interference” for anti-bacterial innate responses.References1. Yanai H., et al., Nature 462, 99-103 (2009)2. Yanai H., et al., Proc. Natl. Acad. Sci. USA. 108, 11542- 11547 (2011)3. Negishi H., et al., Nature Immunol. 13,659-666 (2012)4. Yanai H. et al., Trends Immunol. 33, 633-640 (2012)5. Koshiba R. et al., Biochem Biophys Res Commun., 430, 95-100 (2013)

S-12The TNF Family: Novel Signaling Mechanisms Shared with Other Cytokines, and Unique Functional-RolesDavid WallachDepartment of Biological Chemistry, The Weizmann Institute of Science, 76100 Rehovot, IsraelDespite the overlap in function of the various cytok-ines, and despite their interactions in networks, each cytokine family made unique contribution to our pool of knowledge of the mechanisms of cytokine-mediat-ed immune regulation. Studies of TNF, and of other members of its family, were the first to reveal regula-tion of cell-death via dedicated signaling pathways and to point out roles of cytokines in several other processes of tissue destruction and construction. They also disclosed several important novel molecular mechanisms of signaling, later found to be shared with many other inducers, and to serve crucial roles in the regulation various important biological functions. Particular attention will be given in my talk to the various signaling functions of caspases, proteases whose role as mediators of cytokine-induced signaling was discovered in exploring the mechanisms of death induction by receptors of the TNF family.

S-13Transcriptional Cascades Associated with Inflammatory and Innate Immune ResponsesStephen T. SmaleDavid Geffen School of Medicine at UCLA, Los Angeles, California, USA Macrophages and many other cell types respond to diverse extracellular stimuli by activating the tran-scription of hundreds of genes in a defined temporal and stimulus-specific manner. The transcriptional cas-cade is typically orchestrated by several signal trans-duction pathways, which target transcriptional regula-tors and co-regulators; these factors target genes that are assembled into one of several chromatin states that confer susceptibility to activation. A major goal of our research is to understand how signaling path-

ways, transcriptional regulators, and chromatin struc-ture act in concert to direct a stimulus-specific tran-scriptional cascade. Our current studies derive great benefit from recent advances in high-throughout RNA sequencing (RNA-seq). In particular, by performing RNA-seq with nascent transcripts isolated from chro-matin, it has been possible to rapidly and easily define transcriptional cascades at a global scale with an unprecedented level of precision and quantitation. The high-resolution temporal cascades have revealed clus-ters of co-regulated genes, whose regulatory mecha-nisms have then been evaluated in greater depth. In addition to basic knowledge of the molecular mecha-nisms regulating transcriptional cascades, these stud-ies are facilitating efforts to elucidate mechanisms responsible for the differential or aberrant regulation of gene expression in specific physiological settings and disease states.

S-14Compartmentalized and Systemic Control of Tissue Immunity by CommensalsY. Belkaid and S.NaikMucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda 20892, USA.The body is composed of various tissue microenviron-ments with finely tuned local immunosurveillance systems, many of which are in close apposition with-distinct commensal niches. Mammals have formed an evolutionary partnership with these microbes that is critical for metabolism, tissue development, and host defense. Despite our growing understanding of the ramifications imposed by this host-microbe alliance on immunity, the degree to which individual microen-vironments are controlled by resident microbiota remains unclear. We will discuss how outside of the GI tract, resident commensals can control unique physiological niches and the potential implications of this dialogue for the establishment of immune homeo-stasis, protective responses, and tissue pathology.

S-15Innate DNA Sensing and IFN Induction during Viral Infections.Søren R. Paludan , Aarhus University, Aarhus, Denmark Viruses carrying their genetic information in the form of DNA in all or parts of the viral replication cycle include important human pathogenic viruses like her-pesviruses, adenoviruses, retroviruses, and hepadnavi-ruses. Recently it has emerged that microbial DNA is a potent stimulator of innate immune responses including interferon (IFN) production. Several intrac-ellular and endosomal DNA sensors have been identi-fied. Despite this, there is still limited knowledge on how and where in the cell viral DNA is sensed by the innate immune system, how downstream signaling is


activated, how viruses seek to evade these responses, and also the impact of DNA sensing on antiviral responses in vivo. In this talk, I will present the cur-rent knowledge on how DNA viruses stimulate IFN responses and discuss how this translates to antiviral responses, including the interaction with other innate immunological sensing systems.

S-16CYTOKINE CONTROL OF REGULATORY B10 CELL FUNCTIONThomas F. TedderDepartment of Immunology, Duke University Medical Center, Durham, NC 27710, USAA rare but specific subset of IL-10-competent regula-tory B cells has been identified in mice and humans by their ability to secrete IL-10. We have labeled these B cells as “B10 cells” to identify them as the exclusive source of B cell IL-10. The capacity of B10 cells to produce IL-10 is central to their ability to neg-atively regulate inflammation and autoimmune dis-ease as well as adaptive and innate immune responses. B10 cells are not overtly immunosuppressive, but instead have antigen-specific regulatory functions. Appropriate B cell antigen receptor specificity and signals are required to drive B10 cell development and acquisition of IL-10 competence under physiolog-ical conditions in vivo. Following antigen-specific B10 cell development, their maturation into functional IL-10-secreting effector cells in vivo requires IL-21 and CD40-dependent cognate interactions with anti-gen-specific T cells (Yoshizaki et al. Nature 2012: 491:264-268). These critical checkpoints are likely to direct localized B10 cell IL-10 production to blunt antigen-specific T cell responses during cognate B10:T cell interactions. These findings likely explain how antigen-specific B10 cell effector function can exert such potent in vivo effects and selectively inhibit antigen-specific T cell function during inflammation and autoimmunity without untoward immunosuppres-sion. Insights into the molecular pathways that regu-late antigen-specific B10 cell function in vivo have led to the development of an in vitro culture system that expands functionally-active mouse B10 cells (B10 effector cells) ex vivo by >1,000,000-fold. B10 effector cells resulting from this culture system secrete IL-10, retain their antigen-specific regulatory functions, and have demonstrated potent anti-inflam-matory effects that effectively treat mice with estab-lished autoimmune disease. Thus, autologous B10 effector cells may provide a new therapy for treating refractory autoimmune disease or transplant rejection, particularly for individuals for whom effective thera-pies have not been identified. Supported by NIH grants AI56363 and AI057157 and the Lymphoma Research Foundation.

S-17The Regulation and Function of Interleukin-22 In Epithelial Homeostasis and Host Defense Celine Eidenschenk, Xiaoting Wang, Sascha Rutz, Neko Ota, Kit Wong, Patricia Valdez, Yan Zheng, Wenjun Ouyang. Genentech, Inc. South San Francisco, California USAIL-22 is an IL-10 family cytokine. T cells and innate lymphocytes (ILCs) are the major sources of IL-22. Many pathways, such as IL-23, IL-6, IL-21 and Notch, can regulate IL-22 expression from T cells and ILCs. On the other hand, IL-22 receptor is preferen-tially expressed on various epithelial cells. Upon bind-ing to its receptor, IL-22R1 and IL-10R2, IL-22 regu-lates epithelial innate host defense, epithelial homeo-stasis and wound healing responses. IL-22 is indis-pensable during the early stage of Citrobacter rodenti-um infection, IL-22 is primarily induced by IL-23 from various ILCs. Interestingly, lymphotoxin (LT) pathway is also required for the expression IL-22. IL-22 bridges the LT pathway with intestinal host defense mechanisms. Both LT and IL-22 pathways are required for the maintenance of various GALT such as ILFs and colonic patches during C. rodentium infec-tion in the colon. Therefore, IL-22 not only induces the expression of antimicrobial peptides that control the dissemination of bacteria but also helps the main-tenance of the intestinal integrity. In contrast to its tis-sue protective function in many organs, during Toxoplasma gondii (T. gondii) infection, IL-22 con-tributes to ileitis and epithelial necrosis. In IL-22 defi-cient mice, the epithelial necrosis is completely abol-ished which is also associated with reduced Th1 immunity. IL-18 is a direct target gene that induced by IL-22 from small intestine epithelial cells. IL-18 can also enhance IL-22 production from both T cells and ILCs. Thus, during T. gondii infection, IL-22 and IL-18 form a positive feedback loop which amplifies the Th1 mediated inflammation and tissue damage.

S-18Immunobiology of Single-Chain and Heterodimeric IL-35 Cytokines: Role in Induction of Regulatory B Cells (Breg) and Suppression of CNS Autoimmune DiseaseCharles EgwuaguNational Institutes of Health, Bethesda, Maryland USA The IL-12 family of cytokines is comprised of four heterodimeric cytokines, IL-12, IL-23, IL-27 and IL-35 that play crucial roles in regulating the differen-tiation, growth and functions of lymphocytes. While some members (IL-12 and IL-23) have been implicat-ed in the pathogenesis of several chronic inflammato-ry diseases, others (IL-27 and IL-35) are thought to contribute to mechanisms that mitigate autoimmune diseases. Each IL-12 family cytokine is comprised of an alpha and a beta chain structurally related the IL-6


super-family and cytokine type 1 receptor, respective-ly. We have genetically engineered each alpha and beta subunit of IL-12 family cytokine and novel com-binations of these subunits. Here the focus is on the immunobiology of recombinant IL-35 and its constit-uent subunits, p35 and Ebi3. We describe a novel function of IL-35 in B cells and the use of IL-35-stimulated B cells in ameliorating the CNS autoim-mune disease, Uveitis.

S-19T Cell Activation, Differentiation and Plasticity in Humans Federica SallustoInstitute for Research in Biomedicine, Bellinzona, SwitzerlandThe effectiveness and robustness of the immune response is dependent on different types of effector and memory T cells capable of migrating to different tissues and of producing a variety of cytokines in response to diverse types of pathogens. In principle this response could be built on multiple clones, each performing a given function and/or on distinct descendants of single clones performing multiple functions. We are defining the lineage relationship between different memory T cell subsets and between T helper cells with polarized or mixed cytokine profiles, and the natural and therapeutic plasticity of effector and memory T cells at different stages of differentiation. The study builds on our knowledge of human T cell differentiation and on the identification of different types of effector and memory T cell subsets, as well as on our early studies on the epigenetic control of human CD4 T cell polarization and plasticity. We combine multiparametric flow cytometry and cell sorting, high throughput T cell cloning, and next generation sequencing to analyse the human antigen-specific immune repertoire at the clonal level. Data will be presented on the distribution of effector and memory T cells within individual expanded clones of antigen-specific T cells primed in vivo by different commensals and pathogens, or self antigens and allergen. The data are used to define the lineage relationship of effector and memory T cell subsets, such as T cells producing IFN-γ, IL-4, IL-17 and IL-22, alone or in different combinations, or circulating follicular helper T cells and central memory and effector memory T cells. We expect that these studies will significantly expand our basic understanding of T cell biology and will have translational implications for vaccination and immunotherapy.

S-20Cancer Immunoediting: Basic Mechanisms and Therapeutic ImplicationsRobert D. SchreiberDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

Cancer Immunoediting is the process by which the immune system controls and shapes cancer. We origi-

nally envisaged and subsequently showed that, in its most complex form, cancer immunoediting occurs in three phases: Elimination (i.e., cancer immunosurveil-lance—the host-protective phase of the process); Equilibrium (i.e., immune mediated tumor dorman-cy—the phase in which tumor cells that survive elimi-nation are subjected to immunologic growth control and undergo editing); and Escape (i.e., the phase where immunologically sculpted or immunoselected tumors with either reduced immunogenicity or enhanced immunosuppressive capacity emerge to become clinically apparent, progressively growing tumors). Strong experimental data supporting each phase of the process have been obtained using mouse models of cancer and compelling clinical data have revealed that a similar process also occurs in humans. Our efforts now focus on elucidating the molecular and cellular mechanisms that underlie each phase of cancer immunoediting and in identifying the critical checkpoints that regulate progression from one phase of the process to the next. This focus led to develop-ment of a novel method of cancer exome sequencing and its use in defining mutational tumor antigens as key targets for adaptive immunity in nascent develop-ing unedited cancers. Furthermore, we showed that immunoselection is a major immunoediting mecha-nism. We are now applying this approach to identify-ing mutational antigens in clinically apparent, edited tumors that can be used as targets for different forms of cancer immunotherapy including checkpoint block-ade therapy. Our long-term goal is to develop rapid, safe, specific and effective personalized cancer immu-notherapies.

S-21Loss of Cutaneous TSLP Dependent Immune Responses Skews the Balance of Inflammation from Tumor-Protective to Tumor-PromotingMatteo Di Piazza, Craig Nowell, Ute Koch, André-Dante Durham, and Freddy RadtkeEcole Polytechnique Fédérale de Lausanne, School of Life Sciences, Swiss Institute for Experimental Cancer Research, Lausanne, Vaud, 1015; Switzerland.Inflammation can promote or inhibit cancer progres-sion. We have addressed the role of the pro-inflamma-tory cytokine Thymic Stromal Lymphopoietin (TSLP) during skin carcinogenesis. Using conditional loss- and gain-of-function mouse models for Notch and Wnt signaling respectively, we demonstrate that TSLP mediated inflammation protects against cutaneous car-cinogenesis by acting directly on CD4 and CD8 T cells. Genetic ablation of TSLP receptor (TSLPR) per-turbs T cell mediated protection and results in the accumulation of CD11b+Gr1+ myeloid cells. These promote tumor growth by secreting Wnt ligands and augmenting β-catenin signaling in the neighboring epithelium. Epithelial specific ablation of β-catenin prevents both carcinogenesis and the accumulation of


CD11b+Gr1+ myeloid cells, suggesting tumor cells initiate a feed-forward loop that induces pro-tumori-genic inflammation.

S-22Novel Technologies to Target STAT3: Transition into the ClinicHua YuBeckman Research Institute at City of Hope Comprehensive Cancer Center, STAT3 is crucial for signaling of many cytokines and it is persistently activated in many types of tumors. It plays a crucial role in tumor invasion and resistance to therapy, enabling tumor growth while turning off the body’s anti-tumor immune response. Inhibiting STAT3 could therefore have significant implications for improved cancer therapy. However, as a transcrip-tion factor lacking its own enzymatic activity, STAT3 is a challenging target for conventional small-mole-cule drugs. We have recently developed two technolo-gy platforms to target STAT3: one via siRNA and the other by cell-penetrating antibodies. By covalently linking siRNA to the CpG moiety, we are able to deliver siRNA to those cells expressing the endosomal Toll-like receptor 9 (TLR9), which recognizes CpG. These include immune cells such as dendritic cells, macrophages and B cells, and a variety of tumor cells, including lymphoma and glioma. In addition to serv-ing as a delivery vehicle for the siRNA, CpG’s bind-ing and activation of the TLR9 receptor has its own anti-tumor immunostimulatory effects. The CpG-Stat3 siRNA serves as an ideal weapon against many can-cers, delivering a dual blow by simultaneously acti-vating immune cells in the microenvironment and promoting tumor self-destruction. We are moving this approach towards clinical trials at City of Hope Comprehensive Cancer Center. Another exciting approach to inhibit STAT3 is by cell-penetrating anti-bodies. We demonstrate that attachment of specifical-ly-modified nucleic acid to antibodies enables effi-cient antibody cellular internalization and target rec-ognition. Both local and systemic deliveries of the modified antibodies effectively inhibit STAT3 activity in tumors, resulting in tumor cell apoptosis and tumor regression in various models. We are improving this methodology with the intention to take it the clinic in the near future.

S-23Progressive Recruitment of STAT5 and Establishment of Unique H3K4me3 Marks during Pregnancy Define Mammary-Specific GenesLothar Hennighausen, Keunsoo Kang, Daisuke Yamaji and Gertraud W. RobinsonNational Institutes of Health, Bethesda, Maryland USA.Development of mammary secretory epithelium dur-ing pregnancy is characterized by the sequential acti-

vation of genes that control alveolar epithelial prolif-eration and differentiation, which culminates in the production of milk. These processes are largely con-trolled by the peptide hormone prolactin through the transcription factor STAT5. To uncover molecular mechanisms enabling progressive gene activation dur-ing pregnancy, we explored genome-wide STAT5 binding and H3K4me3 in undifferentiated and differ-entiated mammary tissues at early pregnancy and par-turition, respectively. These data were integrated with RNA-seq data. STAT5 binding to genes that are spe-cifically induced during pregnancy was limited in immature mammary tissue but increased sharply in functional tissue. This increase was associated with the establishment of H3K4me3 marks and transcrip-tional activation. In contrast, bona fide STAT5 target genes that are expressed in a range of cell types were recognized by STAT5 in both immature and mature mammary tissue. STAT5 binding preceded the forma-tion of H3K4me3 marks in some genes suggesting that STAT5 is an early step in establishing transcrip-tion.

S-24CYTOKINE REGULATION OF THE MOLECULAR BALANCE BETWEEN T-BET AND BCL-6 IN EFFECTOR CELL RESPONSESKenneth J. Oestreich, Sarah E. Gilbertson, and Amy S. WeinmannDepartment of Immunology, University of Washington, Seattle, WA USAHelper T cell lineage-specifying transcription factors are often times expressed in more helper T cell sub-types than only the one that it classically defines, and in many cases, the co-expression of these factors is functionally important for influencing the fate of the cell. This raises the intriguing question of how the expression levels and functional activities of the help-er T cell lineage-specifying transcription factors are regulated by the cytokine environment in order to cre-ate the specialized gene expression patterns for each helper T cell subtype. Our research explores this topic by defining the mechanisms that control the interplay between T-bet and Bcl-6 and how this contributes to the underlying gene expression potential of the cell. Notably, the molecular balance between T-bet and Bcl-6 is regulated by environmental IL-2 conditions and this creates flexibility between Th1 and Tfh-like gene programs. Additionally, the IL-2-sensitive regu-lation of the molecular balance between T-bet and Bcl-6 also plays a role in regulating aspects of cell cycle checkpoint control. The mechanistic properties that T-bet and Bcl-6 utilize to impact cell cycle check-point regulation have implications in the functioning of several immune cell types as well as in the patho-genic outcome associated with blood cancers.


S-25C-Type Lectin Receptors (CLRs), Pattern Recognition Receptors for Sensing Fungal Infection and their SignalingXin Lin, Department of Molecular and Cellular Oncology and Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA

Fungal infection, such as Candida Albicans infection, can be life-threatening for immunocompromised indi-viduals. Emerging data indicate that C-type lectin receptors (CLRS) play critical roles as pattern recog-nition receptors (PRRs) for sensing fungal. Recent studies indicate that multiple CLRs including Dectin-1, Dectin-2, infection Dectin-3 and Mincle recognize different components on the cell wall of fungi. We have recently shown that Dectin-3 (also called CLECSF8, MCL or Clec4d), a previously uncharacterized CLR recognized α-mannans on the surfaces of C. albicans hyphae and induced NF-κB activation leading to induction of various pro-inflam-matory cytokines. Mice with either blockade or genet-ically deleted Dectin-3 were highly susceptible to C. albicans infection. In addition, our studies show that Dectin-2 and Dectin-3 constantly formed heterodim-ers for recognizing α-mannans on the surface of C. albicans hyphae. Compared to their respective homodimers, Dectin-2 and Dectin-3 heterodimers bind to α-mannans more effectively, leading to potent inflammatory responses against fungal infections, Together, our study demonstrates that Dectin-2 and Dectin-3 forms a heterodimeric PPR for sensing fun-gal infection and suggests that different CLRs may form hetero- and homo-dimers which provide differ-ent sensitivity and diversity for host cells to detect various microbial infections.

S-26The Good and Evil Faces of the Tyrosine Kinases: Implications for ImmunotherapyThomas A. WaldmannNational Institutes of Health, Bethesda, Maryland USAInterleukin-15 a common gamma cytokine that signals through JAK1/JAK3/STAT5 and that activates anti-tumor T and natural-killer cells, has potential applica-tions in cancer immunotherapy. When IL-15 was administered at 20 µg/kg/day by continuous intrave-nous infusion for 10 days to nonhuman primates there was an 80-100-fold expansion of circulating CD8+ effector memory T cells and an eight-fold increase in the number of NK cells. Based on these experiments we performed a first-in-human phase I dose escalation trial of Escherichia coli (E. coli) produced rhIL-15 in patients with metastatic malignancy. Flow cytometry of peripheral blood lymphocytes revealed that NK and memory T-cells disappeared from blood within min-utes upon IL-15 administration. Subsequently IL-15 treatment produced an eightfold expansion of NK

cells and a twofold expansion of CD8+CD45RO+ memory T-cells. Disorders of gamma cytokines including IL-15 participate in the pathogenesis of autoimmune disorders and T-cell malignancies includ-ing HTLV-1 associated adult T-cell leukemia. The HTLV-1 Tax protein transactivated two autocrine (IL-2/IL-2R alpha, IL-15/IL-15R alpha) and one para-crine (IL-9) pathway that signal through JAK1/JAK3/STAT5 that in turn was associated with ex vivo spon-taneous proliferation of leukemic cells. To further examine the JAK signaling system we performed a molecular interference analysis of target cytokine dependent ATL cell lines using a library of retroviral vectors for inducible expression of short-hair pin RNAs. When this loss of function genetic screen was applied to cytokine dependent ATL cell lines JAK1 was shown to be critical in the survival of cytokine dependent ATL cell lines studied. We evaluated the JAK3/2 inhibitor tofacitinib and the JAK1/2 inhibitor ruxolitinib on cytokine dependent ex vivo proliferation from patients with smoldering and chronic types ATL. These JAK inhibitors dramatically inhibited the ex vivo proliferation. On the basis of these preclinical studies we have initiated a phase II trial evaluating the safety and efficacy of the JAK1/2 inhibitor ruxolitinib in patients with smoldering and chronic ATL.

S-27Natural Killer Cell Memory- Role of Cytokines and Co-Stimulatory ReceptorsLewis L. LanierUniversity of California San Francisco, CA USANatural killer (NK) cells have traditionally be considered cells of the innate immune system, but recent findings suggest that they share many characteristic in common with adaptive immunity. Using a mouse model of cytomegatovirus infection, we have demonstrated that NK cells are capable of undergoing CMV-specific clonal expansion, contraction after control of the infection, and the generation of long-lived “memory” NK cells with an enhanced secondary response to infection. We have investigated the cytokines, signaling molecules, and co-stimulatory receptors that are required for the optimal generation and maintenance of memory in the NK cell lineage.

S-28The beta common cytokine receptor family: Structural insights and signalling mechanismsAngel F Lopez1, Timothy R Hercus1, Sophie E Broughton2, Matthew Hardy3, Barbara J McClure1, Tracy L Nero2, Mara Dottore1, Urmi Dhagat2, Samantha J Busfield3, Gino Vairo3, Nicholas J Wilson3, Andrew D Nash3 and Michael W Parker2. 1 Centre for Cancer Biology, SA Pathology, Adelaide, SA, Australia. 2 St Vincent’s Institute of Medical Research, Fitzroy, Vic, Australia. 3 CSL Ltd, Parkville, Vic, Australia.


The beta common family of cytokines comprises GM-CSF, IL-3 and IL-5, all products of T cells released following activation. These cytokines and their receptors link immunity to the hemopoietic sys-tem and play a significant role in immunopathology and haematological malignancies caused by excessive cytokine production or abnormal beta common recep-tor expression or signalling. It is therefore important to develop a detailed understanding of the structural and functional interactions of the beta common cytok-ines with their receptors in order to devise novel ther-apeutic strategies. The beta common family is part of the Type I cytokine receptor superfamily that encom-passes also the IL-2, IL-4, IL-6, IL-7, IL-9, IL-13, and IL-15 receptors. This family is characterized by their utilization of unique subunits for initial cytokine rec-ognition (alpha chains) and of shared subunits (beta common and gamma common) for signalling. Signalling requires dimerization of the alpha and beta common subunits, that, at least in the GM-CSF recep-tor, leads to the formation of high order complexes, with a dodecamer arrangement representing the mini-mal signalling unit (1). We have now solved the struc-ture of the human IL-3 receptor, the last member of beta common family for which detailed structural information was missing, which, intriguingly, shows both, “open” and “closed” conformations probably reflecting a dynamic state of its N-terminal domain. The IL-3 receptor was crystallised in complex with the monoclonal antibody CSL362, a humanised ver-sion of the blocking (2) and anti-leukaemic (3) anti-body 7G3 to IL-3Ralpha, that has been optimised for NK cell-mediated killing for the treatment of acute myeloid leukaemia (Clinical Trials. Gov. identifier: NCT01632852). The structure of the IL-3 receptor will be presented together with functional data that point to the mechanism of IL-3 recognition and recep-tor signalling.(1) Hansen et al, Cell 134:496-507, 2008(2) Sun et al, Blood 87:83-92, 1996(3) Jin et al, Cell Stem Cell 5:31-42, 2009 S-29Inflammasomes, in Dysbiosis, Health and DiseaseRichard A. Flavell1, 21Department of Immunobiology and 2Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA Inflammasomes are multiprotein complexes that func-tion as sensors of endogenous or exogenous damage-associated molecular patterns. Inflammasomes are now recognized as a cornerstone of the host’s intracel-lular surveillance machinery. We recently identified that deficiency of the NLRP6 inflammasome in mouse colonic epithelial cells results in reduced IL-18 levels and altered fecal microbiota characterized by expanded representation of the bacterial phyla

Bacteroidetes (Prevotellaceae) and TM7. Importantly, NLRP6 inflammasome-deficient mice were character-ized by spontaneous intestinal hyperplasia, inflamma-tory cell recruitment, and exacerbation of chemical colitis induced by exposure to dextran sodium sulfate (DSS). Cross-fostering and cohousing experiments revealed that the colitogenic activity of this microbio-ta is transferable to neonatal or adult wild-type mice, leading to exacerbation of DSS colitis via induction of the cytokine, CCL5. Antibiotic treatment and electron microscopy studies further supported the role of Prevotellaceae as a potential key representative of this microbiota-associated phenotype. There is a very strong association between inflammation and cancer. As we found that dysbiosis drove inflammation in the face of NLRP6 inflammasome deficiency we have investigated whether dysbosis can play a role in the development of cancer. We found indeed that dysbio-sis increased both the number and mass of colon car-cinomas tumors. The mechanism which drove this emanated from dysbiosis leading to the recruitment of inflammatory cells to the intestinal epithelium. The cells secreted interleukin 6 which drove the prolifera-tion of transformed epithelial cells leading to enhanced cancer. It will be worthwhile to investigate the role of dysbiosis in a variety of human cancers


AAbrignani, S., 311Aderem, A., 298Apelbaum, A., 301Artis, D., S-8Auger, J.L., 299Azechi, S., 315

BBabon, J., 302Bagos, A., 318Balfour, Jr., H.H. 299Barak, V., 309Barbieux, I., 308Belkaid, Y., S-14Bekisz, J., 317Belz, G., 302Bianco, A., 311Biancotto, A., 325Bilgic, H., 299Binstadt, B.A., 299Bird, N., 302Bonatto, R.C., 314Boshuizen, M.C.S., 300Bottini, N., 299Braselmann, S., 318Broughton, S.E., S-28Busfeld, S.J., S-28

CCampbell, A.M., 299Caplazi, P., 330,333Carpi, M.F., 314Cataldo, I., 328Chan, A.C., 299Chandrashekaran, I., 302Chappell, C.P., 334Chen, B-C., 305Chen, K., 334Chen, R., 303Chen, Y-C., 306Chen, Y-H., 306Cheng, G., 299Cheong, J.H., 331Choi, B-I., 315

Choy, C., 318Chung, C-L., 305Clark, E.A., 334Clor, J., 304Coniglio, L., 332Corbett, J.A., 299Coyne, C., 322Crosti, M.C., 311Curtsinger, J.M., 299

DDabelic, R., 298Dabydeen, S., 313Day, B., 302De Arujo Júnior, J.P., 314De Caterina, R., 328De Francesco,R., 311De Oliviera Klefens, S., 314De Pace, D., 328De Winther, M.P.J., 300Dhagat, U., S-28Di Piazza, M., S-21Di Scala, R., 328Diamond, M.S., 298Diaz-Cruz, E.S., 313Dixit, V.M., S-10Dong, L., 319Dottore, M., S-28Draves, K.E., 334Duncton, M., 318Durham, A-D., S-21

EEgwuagu, C., S-18Eitson, J.L., 298Eliashar, E., 309Elidan, J., 309Elliott, R.M., 298Endsley, J., 320

FFacciotti, F., 311Fatakdawala, T., 335Fereidouni, M., 316Ferriera, J., 335

Fioretto, J.R., 314Flavell, R.A., S-29Frascoli,M., 332Frances, R., 318Furth, P.A., 313

GGadina, M., 325Gainey, M.D., 298Garcia-Sastre, A., 298Geginat, J., 311Gijbels, M.J.J., 300Gilbertson, S.E., S-24Giltiay, N.V., 334Goldbach-Mansky, R., 325Gollwitzer, E., 307Grogan, J.L., 330, 333Gross, M., 309Gruarin, PP. 311

HHardy, M., S-28Harris, K.G., 322Hasegawa, K., 299Hassankiade, S.N., 316Hearnden, C.H.A., 312Heim, J., 308Hennighausen, L., 313, 327, S-22Hercus, T.R., S-28Holland, S.J., 318Hollander, M.R., 300Hooper, L.V., 326Horrevoets, A.J.G., 300Hsu, W., 303Huang, J., 319Huang, Y., 325Hwang, S-H., 326

IImanaka, N., 298Iwakura, Y., 315Iwakura, Y., 321

JJacques, Y., 308Ji, S., 319Jiang, J., 329Jin, T., 329

KKadoki, M., 321Kakuta, S., 315Kamiya, T., 321Kang, K., 313, 327, S-23Kang, T.J., 331Kanno, S., 317Kaplan, D.H., 334Kedzierski, K., 302Kedzierski, L., 302Kim, S.H., 331Klimpel, G., 320Koch, U., S-21Kolesnik, T., 302Krietsch, J., 311Kubo, S., 315Kurokawa, C.S., 314

LLanier, L.L., S-27Lavelle, E.C., 312Lavoie, T.B., 335Lee, G.S., 331Lee, K.M., 331Lee, W.P., 330, 333Ley, K., 299Li, H., 318Lie, W-R., 304Liew, E.F.Y., S-9Lin, C-H., 305Lin, X., S-25Linossi, E., 302Litvac, V., 298Liu, Y., 325Lopez, A.F., S-28Lopez, L.T., 313

MMacDuff, D.A., 298

AUTHOR-ABSTRACT INDEX


MacKenzie, T.C., 332McClure, B.J., S-28McCoy, J.P., 325Mahmoudi, M., 310Manicassamy, B., 298Mar, K.B., 298Marsland, B.J., 307Masuda, E.S., 318Mescher, M.F., 299Mikulski, Z., 299Mirpuri, J., 326Moraes, M., 314Moretto, M.R., 314Morisseau, S., 308Moro, M., 311Mortier, E., 308Moyron, J., 303Murphy, J., 302

NNaik, S., S-14Nakae, S., 315Nakae, S.,324Nambu, A., 324Nash, A.D., S-28Neddermann, P., 311Nero, T.L., S-28Nicholson, S., 302Nicod, L.P., 307Nicola, N., 302Nizzoli, G., 311Norton, R., 302Nowell, C., S-21

OOestreich, K.J., S-24Oida, T., 319Ouyang, W., S-17Owyang, A., 318

PPaludan, S.R., S-15Pappu, R., 330,333Park, G., 318Parker, M.W., S-28Payan, D.G., 318Peretz, T., 309

Perry, A., 329Peterson, E.J., 299Plet, A., 308Pignataro, L., 311Pine, P., 318Pires, R.B., 314

RRabe, S.Z.T., 310Racaniello, V., 298Rachmut, K., 309Radtke, F., S-21Raetz, M., 327Rahnama, M., 310Ramirez-Carrozzi, V., 330, 333Ransom, J., 303Rastin, M., 310Ratushny, A.V., 298Ricci, F., 328Rice, C.M., 298Richardson, R.B., 298Robinson, G.W., 327, S-23Roe, R., 318Romagnani, C., 311

SSallusto, F., S-19Sasaki, Y., 321Sawatzke, K., 299Scheibenbogen, C., 311Schmeling, D.O., 299Schoggins, J.W., 298Schreiber, G., 301Schreiber, R.D., S-20Shaheen, Z.R., 299Shaked, I., 299Shen, S-C., 306Shim, H., 331Shimizu, K., 315Shimizu, S., 315Shlomchik, M.J., 334Shoyama, F.M., 299Singh, R., 318Siu, S., 318Skawinksi, M., 335Smale, S.T., S-13

Smith, G.A., 323Smith, P., 329Snijder, E.J., 298Soto, H., 303Stanford, S.M., 299Stauffer, T., 335Steckel, B., 311Steinfelder, S., 311Stölzel, K., 311Sturge, C., 326Sudo, K., 324Sun, B., 319

TTabasi, N., 310Tai, E., 318Tamzalit, F., 308Tang, C., 321Tang, Q., 332Tanigawa, N., 317Taniguchi, T., S-11Taunton, J., 323Tedder, T.F., S-16Teunissen, P.F.A., 300Toniato,E., 328Torretta, S., Tran, K., 304Trompette, A., 307Tseng, C-L., 305Tsuno, T., 317Tyagarajan, K., 304

UUrbina, N., 319

VVan der Hoeven, N.W., 300Van der Velden, S., 300Van Royen, N., 300Vario, G., S-28Virgin, H.W., 298

WWaldmann, T.A., S-26Wallach, D., S-12Walpita, P., 320Wang, L-Y., 306

Wang, M., 318Wang, Y., 299Weick, A., 311Weinmann, A.S., S-24Weiss, A., 323Wigoda, M., 309Wilheim, S-H., 326Wilson, N.J., S-28Wilson, T., 302

XXiao, T.S., 329Xu, M., 330, 333

YYabe, R., 315Yadava, K., 307Yamaji, D., 327, S-23Yan, D., 330, 333Yang, Y-C., 306Yarden, G., 301Yarovinsky, F., 326Yi, S., 318Yim, D.S., 331Yokoyama, W.M., 298Young, C., 318Yu, H., S-22Yu, X., 330, 333

ZZanjani, B.R., 310Zhang, J., 318Zhang, J., 330, 333Zhou, J., 303Zhou, J., 319Zhou, W., 299Zoon, K.C., 317


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