Innate Immunity

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  1. properdin
    stabilizes alternative C3 convertase allowing for more C3b to be deposited on the pathogen surface
  2. Factor H
    Factor I
    Factor H binds to C3b. This allows for Factor I to bind. I inactivates C3b converting it to iC3b. 
  3. Decay accelerating factor (DAF)
    Binds to the C3b component of the alternative convertase, causing its dissociation and inactivation. 
  4. Membrane co-factor protein (MCP)
    Same function as DAF, but in addition, factor I can bind and inactivate C3b to iC3b. 
  5. C3 convertase
    • structure: Bb-C3 in the plasma
    • function: cleaves C3 depositing C3b on the pathogen surface
  6. alternative C3 convertase
    • structure: Bb-C3b on the pathogen surface
    • function: cleaves C3 depositing C3b on the pathogen surface.
  7. Complement Receptor 1 (CR1)
    • CR1 binds to C3b allowing for opsonization of bacteria
    • On your own cells, it disrupts C3 convertase activity by making it susceptible to Factor I. 
  8. alternative C5 convertase
    • structure: 2 molecules of C3b and 1 molecule of Bb
    • function: cleaves C5 to C5b and C5a
  9. Membrane Attack Complex
    • structure: C5b, followed by binding of C6, C7, C8. C9 is polymerized forming a pore. 
    • function: kills pathogen by allowing water to flow in. 
  10. CD59
    On human cells, CD59 binds to the C5b678 complex and prevents the binding of C9 to form the pore. 
  11. Homologous Restriction Factor
    same function as CD59
  12. S protein
    prevents soluble C5b-6-7 from binding on human cell membranes
  13. clusterin
    prevents soluble C5b-6-7 from binding on human cell membranes
  14. Factor J
    prevents soluble C5b-6-7 from binding on human cell membranes
  15. a2-macroglobulin
    • a protease inhibitor (proteases are produced de novo by bacterium for the purpose of spreading infection)
    • mechanism: protease cleaves the bait region of the a2-macroglobulin, which is then enshrouded by it.
  16. What are the ligands that the following Toll-like receptors bind to (plus where are they located):
    TLR1:TLR2 heterodimer
    TLR2:TLR6 heterodimer
    TLR4:TLR4 homodimer
    • TLR1/TLR2 heterodimer: lipopeptides 
    • TLR2/TLR6 heterodimer: lipoteichoic acid (found in gram positive bacteria)
    • TLR3: double stranded viral RNA
    • TLR4/TLR4 homodimer: lipopolysaccharide (found in gram negative bacteria)
    • TLR5: Flagellin
    • TLR7: single stranded viral RNA
    • TLR8: single stranded viral RNA
    • TLR9: unmethylated CpG-rich DNA
    • TLR10: ??

    • TLR 3, 7, 8, 9 are found on endosomes
    • the rest are found on plasma membranes.
  17. Describe the TLR4/TLR4 pathway:
    • - bacterial LPS is recognized by a complex of TLR4MD2, and CD14
    • - MyD88 binds to TLR4 and initiates a signaling cascade (if TRIF binds, then antiviral type I interferons are produced)
    • - NFkB release, which activates transcription of inflammatory cytokines.
  18. X-linked ectodermal dysplasia and immunodeficiency
    dysfunctional NFkB activation
  19. Paraoxysmal nocturnal hemoglobinuria
    impaired synthesis of HRF, CD59, DAF
  20. Hereditary angioneurotic edema (HANE)
    impaired synthesis of C1 inhibitor
  21. What binds to cause the "rolling effect" for neutrophils?
    selectins (on endothelial cells) binds to s-Lex (on neutrophil)
  22. CD31
    channel in the endothelial cell which allows the neutrophil to move into the site of infection. 
  23. Describe the Lectin Pathway
    • On sensing bacteria, macrophages release IL-6, which causes the release of acute phase proteins (C-reactive protein, and mannose binding lectin) in the liver. 
    • Mannose Binding lectin froms a complex with MASP-1 and MASP2, which binds son the pathogen surface
    • MASP-2 cleaves C4 --> C4b which binds on the pathogen surface
    • MASP-2 cleaves C2 --> C2a, which binds to C4b, forming the classical C3 convertase
    • Now C3 can be cleaved to C3b and be bound on the pathogen surface
  24. Describe the Classical Pathway
    • C1 binds to C-reactive protein
    • this complex can cleave C4 --> C4b and C2--> C2a, thus forming the classical C3 convertase
  25. C1 inhibitory protein (C1INH)
    • disables C1r (remember C1 binds to C-reactive protein as C1q, C1r, C1s). 
    • mechanism: C1r cleaves C1INH forming a covalently bonded intermediate, which is stable
  26. Type I interferon
    activates natural killer cells
  27. NKG2D
    • activating cell surface receptor on natural killer cell that binds to MIC-A and MIC-B of virus infected cells. 
    • Binding causes the NK cell to attack the virus infected cell by releasing lytic granules. 
  28. MIC-A and MIC-B
    • ligand expressed on the surface of virus infected cells. 
    • Binding with NKG2d of the NK cell, causes it to attack the virus infected cell by releasing lytic granules
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Innate Immunity
2012-08-27 05:51:12
Innate Immunity

Innate Immunity terms
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