Background information
The complement component proteins: C2, C3, C4 and C5 are potent anaphyl-atoxins that are released during complement activation. Binding of these proteins to their respective G protein-coupled receptors, C3aR, C1R and C5aR, induces proinflammatory events, such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. Activation of the complement system leads to the formation of C5b-9 terminal complex, and while C5b-9 can promote cell lysis, the sublytic assembly of C5b-9 on plasma membranes causes an opposite result and induces cell cycle activation and survival. C5b-9 can rescue oligodendrocytes from FAS-mediated apoptosis by regulating caspase-8 processing via PI 3-K signaling. C5b-9 may play a pro-inflammatory role in the acute phase of multiple sclerosis, but may also be neuroprotective during the chronic phase of the disease. Complement C5 precursor contains C5a anaphylatoxin. C3a and C5a secretion correlates with pathophysiological phenotypes such as asthma and bacterial meningitis.
