A heat-labile system of enzymes in plasma associated with response to injury. Activation of the complement cascade occurs through two convergent pathways. In the classical pathway the formation of antibody/antigen complexes leads to binding of C1, the release of active esterase that activates C4 and C2 that in turn bind to the surface. The C42 complex splits C3 to produce C3b, an opsonin, and C3a (anaphylatoxin). C423b acts on C5 to release C5a (anaphylatoxin and chemotactic factor) leaving C5b that combines with C6789 to form a cytolytic membrane attack complex. In the alternate pathway C3 cleavage occurs without the involvement of C142, and can be activated by IgA, endotoxin, or polysaccharide-rich surfaces (eg. yeast cell wall, zymosan). Factor B combines with C3b to form a C3 convertase that is stabilized by Factor P, generating a positive feedback loop. The alternate pathway is presumably the ancestral one upon which the sophistication of antibody recognition has been superimposed in the classical pathway. The enzymatic cascade amplifies the response, leads to the activation and recruitment of leucocytes, increases phagocytosis and induces killing directly. It is subject to various complex feedback controls that terminate the response.
Dictionary of molecular biology. 2004.