| • | 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 |
|