immuno #5.txt

  1. What are the three complement pathways?
    • Classical
    • Lectin-binding
    • Alternative
  2. Is complement part of the innate or acquired immunity?
  3. What is required to activate the classical pathway?
  4. What is required to activate the Lectin-binding pathway?
    • Mannose binding lecting (MBL)
    • or Mannose binding protein (MBP)
  5. What is require to activate the alternative pathway?
    Pathogen surface
  6. What is the convergence point for all three complement pathways?
    C3 convertase
  7. What organ produces MBL? How?
    Liver, Macrophage cytokine activation
  8. What binds to the antibody to initiate the Classical pathway?
  9. What binds to the MBL or MBP to initiate the Lectin-binding pathway?
  10. What occurs to initiate the alternative pathway?
    • C3 is automatically cleaved to C3b so it will bind to the pathogen and then bind B.
    • B will then be cleaved by Factor D to become the C3bBb C3 convertase.
  11. What cleaves factor B in the Alternative pathway?
    Factor D
  12. Name the three C3 convertases associated with the three complement pathways
    • 1) Classical: C4b2b
    • 2) Lectin: C4b2b
    • 3) Alternative: C3bBb
  13. What are the four goals of the complement pathways?
    • 1) Lysis
    • 2) Opsonization
    • 3) Inflammation
    • 4) Clear immune complexes
  14. What fragments perform Lysis?
  15. What fragments perform opsonization?
    C3b and C4b
  16. What fragments perform inflammation?
    C3a, C5a, C4a
  17. What fragments perform immunity clearing?
  18. What is Opsonization?
    Catalyzed phagocytosis (C3b, C4b)
  19. What are three main opsonin receptors?
    CR1, CR3, CR4
  20. How are immune complexes cleared?
    • 1) Binding of C3b
    • 2) RBC binding
    • 3) RBC degradation in spleen or RBC phagocytosis by Macrophages
  21. Which is a more potent inflammatory complement factor, C3a, C4a or C5a?
  22. What is formed to lyse cells?
  23. What forms the MAC complex?
    C5b, 6,7,8,9
  24. What happens if there is a deficiency in the C1 inhibitor?
    Excess swelling b/c of active C3a and C5a which are anaphylatoxins and induce inflammation
  25. What occurs with excess DAF and D59 synthesis on RBCs? What binds at those locations?
    • excess complement
    • D59 = MAC complex location
    • DAF = C3/C5 convertase location
  26. What is a prominent disease if the classical pathway is deficient?
  27. What diseases are common with MAC deficiency (C5b, 6, 7, 8, 9)?
    Meningitis and Gonorrhea
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immuno #5.txt
immuno #5