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15 Cards in this Set
- Front
- Back
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Primary opsins in bacterial defense
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IgG, C3b
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Aids in clearance of immune complexes
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C3b
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What activates the classic complement pathway?
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IgG, IgM
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What activates the alternative complement pathway?
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Molecules on the surface of microbes (esp endotoxin from gram-negative bacteria)
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What two mediators prevent complement activation on self-cells?
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C1 esterase inhibitor, decay-accelerating factor (DAF)
[thus deficiencies lead to hereditary angioedema and hemolytic anemia] |
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What complement components constitute the membrane attack complex (MAC)?
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C5b,6,7,8,9
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These complement components neutralize viruses
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C1,2,3,4
(the ones that do not compose the MAC, which attacks bacteria) |
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This complement component opsonizes bacteria
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C3b (so does IgG)
["b" for "binds bacteria"] |
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These complement components mediate anaphylaxis
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C3a, C5a ("a" for "anaphylaxis")
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Hereditary angioedema is caused by this deficiency
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C1 esterase inhibitor deficiency. C1 esterase inhibitor inhibits C1, factor XII, and kallikrein, thus when these go unregulated they can give rise to vasoactive substances. Angioedema is characterized by local swelling in subcutaneous tissues.
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Neisseria bacteremia is caused by this deficiency
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C5-C8 deficiency
(MAC cannot form) |
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Paroxysmal nocturnal hemoglobinuria, which is complement-mediated RBC lysis, is caused by this deficiency
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DAF deficiency (Decay Accelerating Factor). DAF is a GPI-anchored enzyme on the surface of cells that deactivates complement.
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Severe, recurrent pyogenic sinus and respiratory tract infections are caused by this deficiency
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C3 deficiency
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Increased susceptibility to type III HS reactions occurs in this deficiency
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C3 deficiency
[immune complex destruction relies on C3] |
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This complement component is a PMN chemokine
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C5a
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