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32 Cards in this Set
- Front
- Back
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Antigen
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Any molecule that binds specifically to an antibody, also any molecule that can produce peptides that bind specifically to a T cell receptor
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Innate immunity
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Immunity mediated by non-specific cells
Those include: Neutrophils Macrophages Dendritic cells Natural Killer Cells The first protein responders are antibodies and compleent |
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Complement
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A group of proteins found in serum that exist in inactive forms
They are activated by other active complement proteins |
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Complement pathway
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Three ways to start:
Classic - starts with antibody Alternative - self starts Lectin - self starts All thee converge at production of C3 |
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Classic Complement Pathway
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IgM Antibody produced by B-1 cell binds to specific antigen on pathogen surface
C1 complement can now bind to single IgM molecule Complement is activated C1 converts C2 and C4 C4b and C2a bind to surface of pathogen and forms C3 convertase (C4b2a) C3 is cleaved to C3b and binds to pathogen and can cleave other C3 C3a recruits inflammatory cells to site of infection There is opsonization of pathogens by C3b, facilitating uptake and killing by phagocytes C3b also causes C5 cleavage to C5b and C5a. C5a is a more potent chemotaxis C5b causes polymerization with C6, C7, C8 and 9-15 units of C9 to form a pore Then there is perforation of pathogen cell membrane through Membrane Attack Complex (MAC) leading to pathogen death |
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Lectin Complement Pathway
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Mannose-binding lectin binds to pathogen surface
Complement is activated C3 cleaves to C3b and binds to pathogen C3a recruits inflammatory cells There is opsonization of pathogens by C3b, facilitating uptake and killing by phagocytes And there is perforation of pathogen cell membrane leading to pathogen death |
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Alternative Complement Pathway
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Pathogen surface creates local environment conducive to complement activate
C3 cleaves to C3b and binds to pathogen C3a recruits inflammatory cells to site of infection There is opsonization of pathogens by C3b, facilitating uptake and killing by phagocytes And there is perforation of pathogen cell membrane leading to pathogen death |
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IgM
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Immunoglobulin/antibody
Pentamer that lands on surface of bacterium and creates landing pad for complement C1 attachment |
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C3b receptor
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There are several receptors found on macrophages, monocyes, B-cells and such
Mostly they cause phagocytosis when bound by C3b but the receptor on the B-cell is to help get them activated, take in the bacteria and start the antibody response |
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Regulation of complement
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Two types of inactivating factors:
Soluble - inactivate complement on bacterial and host tissues Membrane bound - inactivate complement on host tissues only |
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C1 INH
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C1 inhibitory enzyme
Inhibits C1 complement |
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iC3b
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Inhibitory C3b enzyme
Convertase that prevents more cleavage of C3 |
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C4 binding protein
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Binds to C4b, causing released of C2a from C3 convertase complex.
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Factor I
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Cleaves C4b to prevent the formation of the C3 convertase complex with C2a
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Factor H
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With the help of Factor I, cleaves C3b into iC3b to prevent further cleavage of C3
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DAF
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Membrane bound complement inactivation factor
Dissociates C3 convertase at human cell surfaces to prevent harm |
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MCP
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Membrane bound complement inactivation factor
Dissociates C3 convertase at human cell surfaces and makes them susceptible to cleavage by Factor I Prevents harm to host cell |
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CD59
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Membrane bound complement inactivation factor
Binds to C5b,6,7,8 complex and prevents recruitment of C9 to form the pore |
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Anaphylactoxins
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Complement that alter the vascular endothelium
Ex: C3a, C5a Act on blood vessels to increase vascular permeability Increases permeability allows increases fluid leakage and release of antibodies and complements at the site of infection They recruit inflammatory cells and begin inflammation |
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What is the initial response to extracellular bacteria
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Starts with complement
C3a and C5s recruit inflammatory mediators C3b acts as opsonin for neutrophils and macrophages |
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How does adaptive immunity start?
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Intracellular pathogens infect dendritic cells
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What are some extracellular pathogen associated molecular patterns?
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Lipopolysaccharide (LPS)
Mannose Glycan fMLP (Formylated Methionine-Leucine-Phenylalanine) TLR (Toll-like receptors) |
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Toll Receptors
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10 types of receptors to recognize extracellular and intracellular pathogens. Located on extracellular membrane and nuclear membrane
Binding to different receptors initiates different secondary messenger systems which activates different transcription factors that controls the actions of CD4, CD8 T-cells Cell membrane receptors TLR1, TLR2: Recognized Lipoproteins TLR5: Recognizes flagellin TLR4: Recognizes LPS Internal receptors on nuclear membrane to recognize intracellular pathogens TLR3: double stranded RNA TLR7: single stranded RNA TLR9: CpG DNA of viruses |
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IL-1
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Macrophage Cytokine
Activates vascular endothelium to make it permeable Helps to activate Naive T lymphocytes Causes local tissue destruction around vasculature to get cells out Increases access of effector cells Produces fever systemically by affecting hypothalamus Up regulates IL-6 production |
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TNF-alpha
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Macrophage Cytokine
Activates vascular endothelium to increase permeability Increases entry of IgG, complement and cells to tissue Shuts down venous return to increase fluid drainage to lymph nodes Produces fever systemically Mobilizes metabolites systemically Causes shock systemically |
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IL-6
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Macrophage Cytokine
Upregulates antibody production at site of infection only if B-cell present Increases lymphocyte production in bone marrow Assists in B-cell activation Produces fever systematically Produces acute phage proteins by hepatocytes |
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CXCL8
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Macrophage Cytokine (AKA IL-8)
Steers other immune cells to the site of antigenic challenge Chemotaxic factor recruits neutrophils, basophils and T-cells to site of infection |
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IL-12
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Macrophage Cytokine
Activates NK cells Causes differentiation of CD4 cells into TH1 T-cells |
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What can the chemokines do systemically?
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IL-1, IL-6, and TNF-alpha work systemically
In the liver they increase production of acute phase proteins In bone marrow they increase neutrophil mobilization for phagocytosis In the hypothalamus they increase body temperature to decrease viral and bacterial replication ability In fat and muscles they mobilize energy production for increased body temperature In dendritic cells they stimulate migration to lymph nodes to mature and initiate adaptive immune response |
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What effect does TNF-alpha have on dendritic cells
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It stimulates migration to lymph nodes and maturation
It initiates adaptive immune response |
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Selectin
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Surface protein expressed by endothelial cells
Bind to carbs displayed on the cell membrane of leukocytes causing them to stick to the walls of the blood vessels Causes rolling of the leukocytes allowing it to search for points to exit the blood vessel and enter CT towards site of injury |
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ICAM
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Intercellular Adhesion Molecule
Glycoprotein expressed on endothelial cells and cells of the immune system Induced by IL-1 and TNF-alpha Binds to ligand expressed on leukocytes to help it transmigrate the endothelium into the affected tissue |
