The C3b or C4b bound to the immune complexes or particle surfaces binds to complement receptors C1, C3 and C4. They are then phagocytosed. The C5a product of C5 cleavage increases the number of CR1 molecules on the neutrophil surface ten-fold from 5,000 to 50,000, thereby facilitating phagocytosis. Complement participates in virus neutralization by coating the virus and preventing attachment and subsequent infection of cells. Coated viruses also can be bound by complement receptors on inflammatory cells including neutrophils and macrophages, and this leads to their destruction by phagocytosis or by release of toxic mediators.
Complement facilitates clearance of immune complexes from the body .
Deficiency in complement components that comprise C1, C2 or C4 can predispose a person to the autoimmune disease, lupus erythematosis . This is because when autoimmune complexes are formed, the classical pathway cannot generate C3b to opsonize the complexes. There are only about 100 CR1 molecules on each RBC surface, but there are so many RBCs, they can carry a lot of immune complexes. Complement plays a major role in the inflammatory response . These components are potent mediators called anaphylatoxins that bind to receptors on mast cells and basophils and stimulate release of histamine .