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. 2004 Jan 16;319(2):176–184. doi: 10.1016/j.virol.2003.11.029

Table 1.

Mammalian complement control proteins

Regulator Distribution Function
C1-inh soluble prevents spontaneous activation of C1 and inactivates C1 on surfaces
C4-bp* soluble accelerates decay of classical pathway C3/C5 convertase; factor I cofactor for degradation of C4b
Factor H* soluble accelerates decay of alternative pathway C3/C5 convertase; factor I cofactor for degradation of C3b
Factor I soluble cleaves C3b and C4b to inactive fragments when bound to a regulatory cofactor
CR1 (CD35)* cell-bound accelerates decay of classical and alternative C3/C5 convertase; factor I cofactor for degradation of C3b and C4b
MCP* (CD46) cell-bound cofactor for the cleavage of C3b and C4b by factor I
DAF* (CD55) cell-bound accelerates decay of C3/C5 convertases
CD59 cell-bound prevents MAC formation

C1-inhibitor (C1-inh), C4 binding protein (C4-bp), factor H, and factor I are all soluble proteins that regulate the early stages of complement activation. Complement receptor 1 (CR1), membrane cofactor protein (MCP), and decay accelerating factor (DAF) are membrane-bound proteins that act at the level of C3, a central component of the complement cascade. CD59 is a cell surface protein that prevents formation of the terminal membrane attack complex (MAC) involved in membrane disruption and cell lysis. RCA proteins are indicated by an asterisk.