Copyright © 2010 Pearson Education, Inc. Immune System: Overview The immune system has three types of components Lymphoid tissues Various types of immune

Copyright © 2010 Pearson Education, Inc.

Immune System: Overview

• The immune system has three types of components

• Lymphoid tissues

• Various types of immune cells

• Chemical signals that coordinate responses


Immune System: Functions

• Protects against pathogens

• Bacteria

• Viruses

• Parasites

• Protects against foreign molecules (e.g., toxins)

• Removes dead or damaged cells

• Attempts to recognize and remove abnormal cells


Immune System: Pathologies

• Incorrect immune responses

• Autoimmune disease (e.g., Type 1 diabetes)

• Overactive immune responses

• Allergies

• Lack of immune response

• Immunodeficiency disease (e.g., SCID and AIDS)


Immunity: Two Intrinsic Defense Systems• Innate system responds quickly and consists of:

• First line of defense – skin and mucosae prevent entry of microorganisms

• Second line of defense – antimicrobial proteins, phagocytes, and other cells

• Inhibit spread of invaders throughout the body

• Inflammation is its most important mechanism

• Adaptive defense system

• Third line of defense – mounts attack against particular foreign substances

• Takes longer to react than the innate system

• Works in conjunction with the innate system


Innate and Adaptive Defenses

Figure 21.1

First line

Second line

Third line


Neutrophils Macrophages Plasma cells

Antibodytiter

CytotoxicT cells

Naturalkiller cells

Time (weeks)

Num

ber

of a

ctiv

e im

mun

e ce

lls


Figure 22-11 Innate Defenses (Part 1 of 2)

Innate Defenses

Physical barrierskeep hazardousorganisms andmaterials outsidethe body.

Phagocytesengulf pathogensand cell debris.

Immunologicalsurveillanceis the destruction ofabnormal cells by NKcells in peripheral tissues.

Interferonsare chemical messengersthat coordinate thedefenses against viralinfections.

Duct of eccrinesweat gland Hair

Fixedmacrophage Neutrophil

Freemacrophage

Naturalkiller cell

Lysedabnormalcell

Eosinophil Monocyte

Secretions

Epithelium

Interferons released by activatedlymphocytes, macrophages, orvirus-infected cells


Figure 22-11 Innate Defenses (Part 2 of 2)

Complementsystemconsists of circulatingproteins that assistantibodies in thedestruction of pathogens.

is a localized, tissue-levelresponse that tends tolimit the spread of aninjury or infection.

Inflammatoryresponse

is an elevation of bodytemperature that acceleratestissue metabolism and theactivity of defenses.

Fever

Mast cell

Complement

Lysedpathogen

Body temperature rises above 37.2ºC inresponse to pyrogens

1. Blood flow increased2. Phagocytes activated3. Capillary permeability increased

7. Adaptive defenses activated

4. Complement activated5. Clotting reaction walls off region6. Regional temperature increased

Innate Defenses


First line of defense: Surface Barriers

• Skin, mucous membranes, and their secretions make up the first line of defense

• Keratin in the skin:

• Presents a physical barrier to most microorganisms

• Is resistant to weak acids and bases, bacterial enzymes, and toxins


First line of defense: Epithelial Barriers

• Epithelial membranes produce protective chemicals that destroy microorganisms

• Skin acidity (pH of 3 to 5) inhibits bacterial growth

• Sebum contains chemicals toxic to bacteria

• Stomach mucosae secrete concentrated HCl and protein-digesting enzymes

• Saliva and lacrimal fluid contain lysozyme

• Mucus traps microorganisms that enter the digestive and respiratory systems

• Mucus-coated hairs in the nose trap inhaled particles

• Mucosa of the upper respiratory tract is ciliated

• Cilia sweep dust- and bacteria trapped by mucus away from lower respiratory passages


Second line of defense: Cells and Chemicals

• The body uses nonspecific cellular and chemical devices to protect itself

• Phagocytes and natural killer (NK) cells

• Antimicrobial proteins in blood and tissue fluid

• Inflammatory response enlists macrophages, mast cells, WBCs, and chemicals

Copyright © 2010 Pearson Education, Inc.Figure 21.2a

Second line of defense: Phagocytes

• Macrophages are the main phagocytic cells

• Two general types:

• Macrophages – most derived from monocytes

• Fixed (ex. Kupffer cells in liver)

• Free/mobile - wander throughout a region in search of cellular debris

• Microphages – circulating neutrophils and eosinophils


Second line of defense: Phagocytes

• Neutrophils become phagocytic when encountering infectious material

• Eosinophils are weakly phagocytic against parasitic worms

• Mast cells bind and ingest a wide range of bacteria

• Mast cells are found in the connective tissue and are similar to basophiles

• Originate in the bone marrow

• contain special cytoplasmic granules which store mediators of inflammation


Phagocytes Ingest Foreign Material

Figure 24-4 (2 of 4)

Copyright © 2010 Pearson Education, Inc.Figure 21.2b

(b)

Lysosome

Microbe adheres to phagocyte.

Phagocyte forms pseudopods thateventually engulf the particle.

Phagocytic vesicle isfused with a lysosome.

Microbe in fused vesicleis killed and digested bylysosomal enzymes withinthe phagolysosome, leavinga residual body.

Indigestible andresidual materialis removed byexocytosis.

Phagocytic vesiclecontaining antigen(phagosome).

Residual body

Acidhydrolaseenzymes

Phagolysosome

4

3

2

1

5


Second line of defense: Inflammation

• The inflammatory response is triggered whenever body tissues are injured

• Prevents the spread of damaging agents to nearby tissues

• Disposes of cell debris and pathogens

• Initiate repair processes

• The four signs of acute inflammation are

• Swelling

• Redness

• Heat

• Pain


Inflammation Response

• Begins with chemical “alarm”

• a flood of inflammatory chemicals released into the extracellular fluid

• Macrophages and epithelial cells of boundary tissues have Toll-like receptors (TLRs)

• TLRs recognize specific classes of infecting microbes (even though we consider macrophages to be “non-specific”)

• Activated TLRs trigger the release of cytokines that promote inflammation and attract WBC


Inflammatory Response• Some of the inflammatory mediators

• Histamine – amino acid derivative produced by basophiles and must cell- promote vasodilation

• Kinins – plasma proteins that are activated by tissue injury and promote vasodilation

• prostaglandins (PGs) – promote neutrophil diapedesis

• Leukotrienes – stimulate vasodilation and netrophil cemotaxis

• Complement – set of proteins that promote phgocytosis, activates cells of the immune system

• Colony-Stimulating Factors – hormones that promote WBC count

• Cells that are involved

• WBC, helper T cells, platelets, endothelial cells


Five Steps of Inflammation

1. Macrophages engulf debris and foreign matter

2. Capillaries dilate and become more permeable

3. Foreign matter contained

4. More leukocytes migrate to area

5. Leukocytes clear infection


1. Phagocytosis of Pathogens

• Proteins on microbes bound by macrophages

• Triggers phagocytosis and secretions

• Secretory products trigger subsequent steps


2. Dilation and Increased Permeability in Capillaries

• Damaged mast cells secrete histamine

• Histamine triggers dilation and increases permeability

• Result: increased blood flow and increased movement of proteins and cells to injured tissue


2. Vasodilation and Increased Vascular Permeability

• The most immediate requirement is to bring WBC to the injury site!

• Vasodilation – causes hyperemia (increased blood flow) (Which sign of inflammation?)

• Increase permeability of blood walls (cells separate slightly) – causes edema (leakage of exudate) (Which sign of inflammation?)

• Exudate—fluid containing proteins, clotting factors, and antibodies

• Exudate moves into tissue spaces causing local edema (swelling), which contributes to the sensation of pain


3. Containment of Foreign Matter

• Clotting factors eventually form clot in tissue, prevents spread of foreign matter

• Eventually forms a scab


4. Inflammatory Response: Phagocytic Mobilization• Four main phases:

• Leukocytosis – neutrophils are released from the bone marrow in response to leukocytosis-inducing factors released by injured cells

• Margination – neutrophils cling to the walls of capillaries in the injured area

• Endothelial cells in the injury site produce cell-adhesion molecules that make the surface “sticky” to help in this process

• Diapedesis – neutrophils squeeze through capillary walls and begin phagocytosis

• Chemotaxis – inflammatory chemicals attract neutrophils to the injury site


4. Leukocyte Migration and Proliferation

• 1 hour: neutrophil migration

• 10 hours: monocyte migration macrophages


Fever

• Abnormally high body temperature in response to invading microorganisms

• Maintenance of a body temperature above 37.2oC (99oF)

• The body’s thermostat is reset upwards in response to pyrogens, chemicals secreted by leukocytes and macrophages exposed to bacteria and other foreign substances

• High fevers are dangerous because they can denature enzymes

• Moderate fever can be beneficial:

• Promotes INF activity

• May inhibit some viruses and bacteria reproduction

• Increase body metabolism so enzymatic reactions occur faster and so is tissue repair


Second line of defense: Antimicrobial Proteins

• Enhance the innate defenses by:

• Attacking microorganisms directly

• Interfering with microorganisms’ ability to reproduce

• The most important antimicrobial proteins are:

• Interferon

• Complement proteins


Second line of defense: Interferons – defense against viruses

• Interferons (INF) provide rapid response.

• Produced by a variety of body cells

• Lymphocytes produce gamma (), or immune, interferon

• Most other WBCs produce alpha () interferon

• Fibroblasts produce beta () interferon

• INF alpha and beta are the most potent against viruses

• All three interferons increase expression of class I MHC molecules and thus promote recognition by cytotoxic T cells.

• All three interferons can activate NK cells which can then kill virus-infected cells.


Figure 22-13 Interferons

Alpha ()-interferons areproduced by cells infectedwith viruses. They attractand stimulate NK cells andenhance resistance to viralinfection.

Beta ()-interferons,secreted by fibroblasts,slow inflammation in adamaged area.

Gamma ()-interferons,secreted by T cells and NKcells, stimulatemacrophage activity.


Second line of defense: Interferon (IFN)

• when a host cell is invaded by a virus it activates the genes that synthesize IFN

• Interferon molecules leave the infected cell and enter neighboring cells

• Interferon stimulates the neighboring cells to activate genes for PKR (an antiviral protein)

• PKR nonspecifically blocks viral reproduction in the neighboring cell

• Interferons also activate macrophages and mobilize NKs

• Interferon can not save the infected cell but can prevent the virus from infecting other cells

Copyright © 2010 Pearson Education, Inc. Figure 21.5, step 5

VirusNew viruses

Viral nucleic acid

DNA

mRNA

Nucleus

Interferon

Virusenters cell.

Interferongenes switch on.

Cell producesinterferonmolecules.

Interferonbindingstimulates cell toturn on genes forantiviral proteins.

Antiviralproteins blockviralreproduction.

Host cell 1Infected by virus;makes interferon;is killed by virus

Innate defenses Internal defenses

Host cell 2Binds interferon from cell 1; interferon induces synthesis ofprotective proteins

1

2

34

5


Second line of defense: Complement“complete the action of antibody”

• 30 or so proteins synthesized mainly by the liver

• circulate in the blood in an inactive form and activated in the presence of pathogen

• Proteins include C1 through C9, factors B, D, and P, and regulatory proteins


Second line of defense: Complement system functions

• Destruction of target cells membrane (MAC)

• Stimulation of inflammation – C3a stimulates mast cells and basophils to secrete histamine

• Attraction of phagocytes

• Enhancement of phagocytosis –

• Phagocytes membrane carry receptors that can bind to the complex of the complement proteins and antibodies.

• The binding results in much more efficient phagocytosis.

• The antibodies in such a complex are called opsonins and the effect is called opsonization (enhanced attachment )


• Are a small, distinct group of large granular lymphocytes

• React nonspecifically and eliminate cancerous and virus-infected cells

• Kill their target cells by releasing perforins and other cytolytic chemicals

• Secrete potent chemicals that enhance the inflammatory response

• NK cells

• Recognize cell surface markers on foreign/abnormal cells

• Recognize variety of antigens (less selective)

• Immediate response when contact abnormal cells

• Destroy cells with foreign antigens

Second line of defense: Natural killer (NK) cells


Properties of specific immunity

• Specificity – activated by and responds to a specific antigen

• Versatility – is ready to confront any antigen at any time

• Memory – “remembers” any antigen it has encountered

• Tolerance – responds to foreign substances but ignores normal tissues


Complete Antigens• Substances that can mobilize the immune system and

provoke an immune response

• mostly large, complex molecules not normally found in the body (nonself)

• Important properties of antigene:

• Immunogenicity – ability to stimulate proliferation of specific lymphocytes and antibody production

• Reactivity – ability to react with products of activated lymphocytes and the antibodies released in response to them

• Complete antigens include foreign protein, nucleic acid, some lipids, and large polysaccharides


Haptens (Incomplete Antigens)

• Small molecules, such as peptides, nucleotides, and many hormones, that are not immunogenic but are reactive when attached to protein carriers

• If they link up with the body’s proteins, the adaptive immune system may recognize them as foreign and mount a harmful attack (allergy)

• Haptens are found in poison ivy, dander, some detergents, and cosmetics


Figure 19.14 2

The formation of an antigen-antibody complexCarriermolecule

Partial antigen(hapten)

Antibody

Antibody

Antigen-antibodycomplex

Antibodies bind not to the entireantigen, but to specific portions ofits exposed surface—regionscalled antigenic determinantsites.

A complete antigen is anantigen with at least two antigenicdeterminant sites, one for each ofthe antigen binding sites on anantibody molecule.

Partial antigens, or haptens, do notordinarily cause B cell activation.However, they may become attached tocarrier molecules, forming combinationsthat can function as complete antigens.The antibodies produced will attack boththe hapten and the carrier molecule. Ifthe carrier molecule is normally presentin the tissues, the antibodies may beginattacking and destroying normal cells.This is the basis for several drugreactions, including allergies topenicillin.


Cells of the Adaptive Immune System

• Two types of lymphocytes

• B lymphocytes – oversee humoral immunity

• T lymphocytes – non-antibody-producing cells that constitute the cell-mediated arm of immunity

• Antigen-presenting cells (APCs):

• Do not respond to specific antigens


Lymphocytes can become immunocompetent

• Immature lymphocytes released from bone marrow are identical

• During their development the lymphocyte:

• Must become able to recognize its one specific antigen – become immunocompetent

• Must be relatively unresponsive to self so it will not attack the body’s own cells – self tolerance

• Location of becoming immunocompetent is the key for a lymphocyte to become B cell or a T cell

• B cells mature in the bone marrow

• T cells mature in the thymus


Immunocompetent B or T cells

• It is genes, not antigens, that determine which foreign substances our immune system will recognize and resist

• Become immunocompetent before they encounter antigens they may later attack

• Immunocompetence - displaying a unique type of receptor that responds to a specific antigen


Immunocompetent B or T cells

• An immunocompetent cell divides rapidly to form a clone of cells with identical receptors. All clones yet to encounter an antigen are called the virgin/naive lymphocyte pool.

• Are exported to secondary lymphoid tissue where encounters with antigens occur

• Mature into fully functional antigen-activated cells upon binding with their recognized antigen

• Clonal selection of B or T cells occurs when antigens bind to their receptors, causing them to proliferate.


Antigen-Presenting Cells (APCs)• Major functions in immunity are:

• To engulf foreign particles

• To present fragments of antigens on their own surfaces, to be recognized by T cells

• Major APCs are

• Dendritic cells (DCs),

• Dendritic cells (DC) are bone marrow-derived cells that are specialized to take up, process and present antigen

• Dendritic cells are present in small quantities in tissues that are in contact with the external environment, mainly the skin (where they are often called Langerhans cells) and the inner lining of the nose, lungs, stomach and the intestines.

• Macrophages that are found all over the body

• Activated B cells


Antigen-Presenting Cells Display Foreign Proteins

Figure 24-4 (4 of 4)


Importance of Cellular and humoral Responses• Importance of Humoral Response (Soluble antibodies)

• The simplest ammunition of the immune response

• Interact in extracellular environments such as body secretions, tissue fluid, blood, and lymph

• Importance of Cellular Response (T-cells)

• T cells recognize and respond only to processed fragments of antigen displayed on the surface of body cells

• T cells are best suited for cell-to-cell interactions, and target:

• Cells infected with viruses, bacteria, or intracellular parasites

• Abnormal or cancerous cells

• Cells of infused or transplanted foreign tissue

Copyright © 2010 Pearson Education, Inc.Figure 21.10

Plasmacells

Secretedantibodymolecules

Clone of cellsidentical toancestral cells

Subsequent challenge by same antigen

MemoryB cell

MemoryB cells

Plasmacells

Secretedantibodymolecules

Secondary Response (can be years later)

Primary Response(initial encounterwith antigen)

Antigen

Antigen bindingto a receptor on aspecific B lymphocyte(B lymphocytes withnon-complementaryreceptors remaininactive)

Proliferation toform a cloneB lymphoblasts


Antibodies

• Also called immunoglobulins

• Plasma cells make over a billion types of antibodies

• makes the gamma globulin portion of blood proteins

• Are soluble proteins secreted by activated B cells and plasma cells in response to an antigen

• Are capable of binding specifically with that antigen

• Antibodies themselves do not destroy antigen; they inactivate and tag it for destruction


Basic Antibody Structure

• Consists of four polypeptide chains linked together with disulfide bonds

• Two identical heavy (H) chains and two identical light (L) chains

• The four chains bound together form an antibody monomer

• Each chain has a variable (V) region at one end and a constant (C) region at the other

• Variable (FAB) regions of the heavy and light chains combine to form the antigen-binding site

• Constant (FC) region Determine the class of the antibody (one of the 5 groups)


Antibody Structure


Classes of Antibodies

• IgD – monomer attached to the surface of B cells, important in B cell activation

• IgM – pentamer released by plasma cells during the primary immune response

• IgG – monomer that is the most abundant and diverse antibody in primary and secondary response; crosses the placenta and confers passive immunity

• IgA – dimer that helps prevent attachment of pathogens to epithelial cell surfaces

• IgE – monomer that binds to mast cells and basophils, causing histamine release when activated


http://www.as.wvu.edu/~rbrundage/chapter12b/sld012.htm

Neutralization – by binding to specific sites on the antigen, the antibody prevents its binding to cells


Actions of antibodies – agglutination and precipitation

• Ab molecules have at least 2 binding sites

• Ag have many antigenic determinant sites

• When Ag are far apart Ab will bind with 2 binding sites to the same antigen

• If Ag are close, Ab can bind to antigenic determinant sites of different Ag.

• As a consequence, the Ab “tie” Ag molecules together. Such a complex is called immune complex

• When the complexes are too big to be soluble they “sink” in a process called precipitation

• When the target Ag are on the surface of the cell or virus the formation of the large complex is called agglutination (example: clumping of RBCs in incompatible blood transfusion)




Complement Fixation and Activation

• Complement fixation:

• Main mechanism used against cellular antigens

• Antibodies bound to cells change shape and expose complement binding sites

• This triggers complement fixation and cell lysis

• Complement activation:

• Enhances the inflammatory response

• Uses a positive feedback cycle to promote phagocytosis

• Enlists more and more defensive elements



Activation of complement (nonspecific reaction) – when antibody bind to antigen, the Ab shape changes and that allows the binding of the complement proteins (which pathway?)


The prevention of bacterial and viral adhesion

• Covered by Ab, pathogens have reduced ability to attach to body surfaces and penetrate.

Fig. 1: Bacterial Adherence Via Pili

Fig. 1A: Blocking Bacterial Adherence with Antibody

Molecules

http://www.cat.cc.md.us/courses/bio141/lecguide/unit3/humoral/abydefense/opsonization/opsonization.html



Phagocytes membrane carry receptors that can bind to the complex of the complement proteins and antibodies. The binding results in much more efficient phagocytosis. The antibodies in such a complex are called opsonins and the effect is called opsonization (enhanced attachment )

Copyright © 2010 Pearson Education, Inc. Figure 21.15

Inactivates by

Antigen Antibody

Fixes and activates

Enhances Enhances Leads to

Phagocytosis

Chemotaxis

Histaminerelease

Inflammation Cell lysis

Agglutination(cell-bound antigens)

Precipitation(soluble antigens)

Neutralization(masks dangerousparts of bacterial

exotoxins; viruses)

Complement

Antigen-antibodycomplex

Adaptive defenses Humoral immunity

Mechanisms of Antibody Action - summary


Immunological Memory• Primary response – the initial response to an antigen

• Cellular differentiation and proliferation, which occurs on the first exposure to a specific antigen

• Lag period: 3 to 6 days after antigen challenge

• Peak levels of plasma antibody are achieved in 10 days

• Antibody levels then decline

• If the antigen is not present anymore, the antibody production decrease. This reduction happens because:

• Plasma cells have short life span (few days)

• Suppressor T cells suppress plasma cells production

• IgM molecules are the first to appear during primary response. IgM provide the immediate defense. This defense is limited because no memory cells are being produced

• IgG – rise slow. Memory cells are formed


• Secondary immune response – re-exposure to the same antigen

• Sensitized memory cells respond within hours

• Antibody levels peak in 2 to 3 days at much higher levels than in the primary response

• Antibodies bind with greater affinity, and their levels in the blood can remain high for weeks to months

• Memory B cells can leave for 20 years or longer

• When a second exposure to antigen occur, memory B cells differentiate into plasma cells

• This response is immediate because memory B cells are activated by relatively low levels of antigen

• The antibody titer rises rapidly and to higher levels than during primary response

Secondary antibody response


The Primary and Secondary Immune Responses

Copyright © 2010 Pearson Education, Inc. Figure 21.13

PassiveActive

Humoralimmunity

Artificiallyacquired

Injection ofimmune serum (gamma globulin)

Naturallyacquired

Antibodiespass from mother tofetus via placenta; or to infant in her milk

Artificiallyacquired

Vaccine;dead or attenuated pathogens

Naturallyacquired

Infection;contact with pathogen


Antigen Recognition and MHC Restriction

• Immunocompetent T cells are activated when the variable regions of their surface receptors bind to a recognized antigen

• T cells must recognize:

• Nonself (the antigen)

• Self (a MHC protein of a body cell)


Specific T-cells roles: Helper T Cells (TH)

• Regulatory cells

• Once primed by APC presentation of antigen, they:

• Chemically or directly stimulate proliferation of other T cells (using protein mediators called lymphokines)

• In the absence of lymphokines the immune system is almost paralyzed

• Without TH, there is no immune response


Lymphokines functions

• Promote the growth and proliferation of other T cells (cytotoxic and suppressor)

• Stimulate B-cells growth and differentiation to plasma cells

• Amplify innate defense mechanisms


Specific T-cells roles: Cytotoxic T Cell (Tc)

• TC cells, or killer T cells, are the only T cells that can directly attack and kill other cells

• They circulate throughout the body in search of body cells that display the antigen to which they have been sensitized

• Their targets include:

• Virus-infected cells

• Cells with intracellular bacteria or parasites

• Cancer cells

• Foreign cells from blood transfusions or transplants


Mechanisms of Tc Action

• Bind to the target cell and release perforin into its membrane

• In the presence of Ca2+ perforin causes cell lysis by creating transmembrane pores

• Secreting lymphotoxin, which fragments the target cell’s DNA

• Secreting gamma interferon, which stimulates phagocytosis by macrophages


Antigen Recognition and the Activation of Cytotoxic T Cells


Other T Cells

• Suppressor T cells (TS) – regulatory cells that release cytokines, which suppress the activity of both T cells and B cells


Self-Antigens: MHC Proteins

• Major histocompatibility complex - MHC proteins, mark a cell as self

• The two classes of MHC proteins are:

• Class I MHC proteins – found on virtually all body cells

• Class II MHC proteins – found on certain cells in the immune response


MHC classes – class I

• Class I – found on all nucleated cells (“hey, I’m an abnormal cell – please kill me”)

• “Sign” infected, sick or abnormal cells that need to be destroyed by the T-cells

• When type I are forming they “pick up” peptides from the cytoplasm and carry them to the cell surface

• If the peptides are normal (healthy cell) the T-cells will ignore them

• If the cytoplasm contain abnormal peptides or viral proteins, T-cells will be activated. This activation will lead to the cell destruction


MHC classes – class I


• Class II MHC proteins are found only on mature B cells, some T cells, and antigen-presenting cells (“Hey, this antigen is dangerous – get rid of it”)

• Class II are found on cells that the body does not need to destroy – it is only a mean to present non-self material

• Phagocytes cells engulf and break down pathogens

• A phagosome containing pathogens (with exogenous antigens) merges with a lysosome

• This antigen processing creates fragments that are bound to type II MHC and inserted into the cell membrane

MHC classes – class II


MHC classes – class II


Cell-Mediated Immune Response

• Two major populations of T cells mediate cellular immunity:

• CD4 cells (T4 cells) are primarily helper T cells (TH)

• CD8 cells (T8 cells) are cytotoxic T cells (TC) that destroy cells with foreign antigens

• MHC restriction – TH and TC bind to different classes of MHC proteins

• TH / CD4 cells bind to antigen linked to class II MHC proteins

• TC / CD8 cells are activated by antigen fragments presented by class I MHC proteins



Presentation of Antigen to T cells


A Summary of the Pathways of T Cell Activation

Documents

Copyright © 2010 Pearson Education, Inc. Immune System: Overview The immune system has three types of components Lymphoid tissues Various types of immune