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The complement cascade is affected by a number of other plasma and tissue-based elements:

  • plasmin can cleave C1 and C3; it may be circulating in plasma or released in the lysosomal contents of neutrophils
  • thrombin can cleave early complement components
  • activated kallikrein, as well as stimulating kinin formation, can trigger complement
  • bacterial proteases can cleave early complement components directly
  • opsonin-bacterial complexes may fix complement and promote its activation

With all the potential for positive feedback and amplification, perhaps it is surprising that the system does not become disordered more frequently. Two examples of excessive activation include rheumatoid arthritis and some forms of glomerulonephritis.

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