The monoclonal antibody 3D5 recognizes complement decline acceleration factor (DAF), also known as CD55. Cells express several proteins on their surface that protect against complement attack, namely C receptor I (CR1), decay acceleration factor, membrane cofactor protein (MCP). CR1, CD55 and MCP regulate the activation pathway of complement by accelerating the degradation of C3 and C5 convertases (CR1, CD55) or acting as cofactors of serine protease factor I. The cleavage of this factor irreversibly inactivates C3b (CR1, MCP).
Mouse CD55 is a 60 kDa transmembrane protein that binds C3b and C4b to inhibit the formation and half-life of C3 convertase. CD55 is widely distributed in cells in contact with serum, including hematopoietic and non-hematopoietic cells. Although CD55 has no important role in controlling hemolysis of red blood cells, it plays an important role in regulating the deposition of C3 on nucleated cells.
CD55 and other complement regulators can protect one's own cells from damage mediated by autologous complement. CD55 and CD46 together prevent the deposition of autologous C3, while CD59 inhibits this pathway at a key endpoint.