No single canonical name—refers to a group, most commonly "Regulators of complement activation". If you need a specific molecule, see entries like "Complement factor H" or "Decay-accelerating factor." (No standard abbreviation for the group; individual proteins do (e.g., CFH for Complement factor H, DAF for Decay-accelerating factor).)

Complement system activation regulators are a diverse group of proteins that tightly control complement activation and prevent host tissue injury caused by accidental or excessive complement activation. They act at multiple points in the complement cascade—including the initial steps, C3/C5 convertase formation, and MAC assembly. Their activities include accelerating the decay of convertase complexes, serving as cofactors for complement component cleavage, and directly inhibiting complex assembly. Dysfunction or absence of these regulators can result in autoimmune diseases, inflammatory tissue injuries, and susceptibility to infections. Examples include complement factor H, decay-accelerating factor (CD55), CD59 (protectin), membrane cofactor protein (CD46), C1 inhibitor (C1-INH), clusterin, and vitronectin. These proteins are major targets both for laboratory investigation and therapeutic intervention in complement-mediated diseases.

Other names

Regulators of complement activationComplement control proteinsRCA proteinsComplement regulatory proteinsSpecific entries: Complement factor H (CFH)Decay-accelerating factor (DAF; CD55)ClusterinVitronectinC1 inhibitor (C1-INH)CD59 (protectin)Membrane cofactor protein (MCP; CD46)C4b-binding protein (C4BP)

Inhibition of complement cascade; Decay-acceleration (dissociation of convertase complexes); Cofactor activity (helping Factor I cleave C3b/C4b); Terminal pathway blockade (inhibition of MAC formation by CD59); Inhibition of complement initiation (C1-INH inhibits C1 complex).