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.