• | classic pathway = antigen-antibody |
• | alternate pathway = contact with bacterial wall lipopolysaccharides etc… (type II and type III reactions) |
• | C3a, C5a = chemotactic factors (for PMN’s, eosinophil’s, and monocytes) |
• | decreased C3 (= active lupus?) |
complement deficiencies:
• | early components --> autoimmune |
• | late components --> infections |
C1 esterase inhibitor | hereditary angioedema |
factor I, C3, factor D | pyogenic infections (abscesses) |
C5, C6, C7, C8 | disseminated gonococcemia |
C5 dysfunction | Leiner’s disease |
decreased C4 | hereditary angioedema |
decreased C1q | acquired angioedema |
decreased C3 and circulating C3 nephritic factor | partial lipodystrophy |
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