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The Immune SystemThe Immune System
1. The Innate System
2. The Adaptive System
The Innate Immune SystemThe Innate Immune System
“Nonspecific” system– Surface Barriers
– Cell and Chemical Responses
Innate Immunity: Surface BarriersInnate Immunity: Surface Barriers
Innate Immunity: Innate Immunity: Cell and Chemical DefensesCell and Chemical Defenses
• They do not target specific pathogens– They target abnormal or foreign cells
• Six categories:– Phagocytes– Natural killer (NK) cells– Inflammation response– The complement system– Interferons– Fever
PhagocytesPhagocytes
• Macrophages, neutrophils, eosinophils
1. Adherence and endocytosis2. Phagocytic endosome3. Lysosome fuses with endosome,
releases hydrolytic acids/enzymes4. Microbe is killed and digested5. Exocytosis
Natural Killer CellsNatural Killer Cells
• Lymphocytes that destroy tumor cells and cells infected with viruses
• Not phagocytes, instead release chemicals onto cell membranes– Cytolytic, perforin complexes
• The target cell lyses & nucleus disintegrates
• NK cells also release substances to stimulate inflammation
Inflammation Inflammation ResponseResponse
•Redness
•Increased Temperature
•Swelling
•Pain
The Complement SystemThe Complement System• > 20 plasma proteins • Activation triggers cascade
of chemical reactions• Molecular Complexes form:
– Membrane Attack Complex creates holes in bacterial cell membranes
– C3b marks them for phagocytes
– C3a and C5a stimulate mast cells to release histamines
InterferonsInterferons - Interfere with viral - Interfere with viral replicationreplication- Block protein synthesis - Block protein synthesis at ribosomesat ribosomes- Activate macrophages- Activate macrophages- Mobilize NK cells- Mobilize NK cells
FeverFever
• When macrophages attack foreign matter, they release chemicals called pyrogens into the blood– Endogenous: interleukins, tumor necrosis factors, macrophage
inflammatory protein, interferons– Exogenous: Lipopolysaccharides of gram-negative bacteria trigger
endogenous factors
• The hypothalamus is stimulated to increase body temperature – fever
• Liver and spleen sequester iron and zinc• High temp. unfavorable for microbes
The Adaptive Immune SystemThe Adaptive Immune System
“Specific” defense mechanisms
• Three characteristics:– recognizes & targets specific foreign
substances– protects the entire body, not a specific
injury or infection site– has a "memory" to store information
from past exposures
Cell RecognitionCell RecognitionProteins, polysaccharides, glycoproteins signal the identity of the cell (host or foreign)
• Major histocompatibility complexes (MHC)– Molecular markers on host cells
• Antigens– Substances that mobilize the immune response
• Molecular markers on foreign cells, abnormal/infected or cancerous host cells
Auto-immune diseases arise when our immune system cannot differentiate “host” from “foreign” cells
Key to Adaptive Immune SystemKey to Adaptive Immune System
• Lymphocytes• Originate from stem cells in bone marrow
• 30% of circulating WBCs
– B cells• mature in Bone marrow
– T cells• mature in Thymus Gland
– Both types are made in the bone marrow– Immune response may be antibody-mediated
(humoral) or cell-mediated
Antibody-mediated ImmunityAntibody-mediated Immunity
• Antibodies: Y-shaped proteins (4 polypeptides) – Made by mature B-
lymphocytes
• Binds to antigens to form antigen-antibody complex
Antibody-mediated ImmunityAntibody-mediated Immunity
• Immunoglobulin classes– IgD: antigen receptor of B cell
– IgM: antigen receptor of B cell (monomer); released by plasma cells during primary response (pentamer)
– IgG: most abundant and diverse; targets bacteria, viruses, toxins; main antibody for both primary and secondary response
– IgA: found in exocrine secretions; prevents pathogens from attaching to epithelial surface
– IgE: bound to mast cells and basophils; mediates inflammation and allergic reaction
Antibody-mediated ImmunityAntibody-mediated Immunity
Antibody-mediated Antibody-mediated ImmunityImmunity
• WBC detects a pathogen or abnormal cell– Attacks pathogen
– Alerts Helper T cells and B cells
• T cells attracted by chemical signals
• B cells alerted by using the pathogen’s own antigens
Antigen
Pathogen
MHC
MHC+Antigen
Signalingmolecules
Helper T cell
B cell
Macrophage
Antibody-mediated Antibody-mediated ImmunityImmunity• Antigens bind to specific
antibodies on B cell surface
• Activation causes B cells to divide rapidly– Plasma cells
• produce antibodies
• 100 million antibodies/hour
– Memory B cells• Remain on “stand by” until
activated by helper T cells
• Surveillance
Cell-mediated Cell-mediated ImmunityImmunity• MHC + antigen
complex waves a warning flag
• Class II MHC’s found on B cells, some T cells, and antigen-presenting cells
• Class I MHC’s found on most cells, except RBCs
Cell-mediated Cell-mediated ImmunityImmunity
AntigenPathogen
MHC
MHC +Antigen
Signalingmolecules
Signalingmolecules
Macrophage
Helper T cell
Cytotoxic T cell
ActivatedCytotoxic T cell
Memory T cell
Perforinmoleculesform poresin pathogencell membrane
• Helper T cells (CD4):– recognize class II MHC– stimulate other immune cells
• Cytotoxic T cells (CD8):– recognize class I MHC– kill infected, cancer, or foreign cells
• Memory T cells:– reactivate on re-exposure
• Suppressor T cells:– suppresses other immune cells
Cell-mediated ImmunityCell-mediated Immunity
• Helper T-cells facilitate both cell-mediated and antibody-mediated immune responses
• Cytotoxic T cells function similar to NK cells, however they only see specific MHC I + antigen complexes
Memory B and T Cells are Like…Memory B and T Cells are Like…
Immune MemoryImmune Memory• Primary immune response
– first exposure to pathogen– recognition, production of B & T cells
• 3 to 6 day lag time• antibodies peak in 10 to 12 days
– B & T memory cells created– basis for "immunity" from the disease
• Secondary immune response– Memory B & T cells immediately identify the
pathogen– faster, longer lasting, more effective than the first– at subsequent infection, new legions of B & T
cells form in a few days– often no symptoms are noticed