Complement is not antigen-specific and it is activated immediately in the presence of a pathogen, hence it is considered as a part of innate immunity.
Complement stimulates inflammation, facilitates antigen phagocytosis, and lyses of some cells directly. Even though pathways of complement activation are different in different conditions, many of the components participating in the effector functions are same.
The fragments of activated components of complement system are called “opsonins”. “Opsonins adhere to micro organisms to promote leukocyte chemo attraction, antigen binding, phagocytosis and activation of macrophage and neutrophil killing mechanisms.
Complement fragments also known as “anaphylatoxins” promote an inflammatory response by binding to complement receptors on mast cells and triggering release of histamine.
Histamines increases blood vessel permeability and smooth muscle contraction. Complement is also important for neutralization of virus and removal of immune complex.
Complement activation stimulates several antimicrobial activities. The end point is formation of a membrane attack complex (MAC), which inserts into lipid membranes of bacteria or eukaryotic cells and causes osmotic lysis.
Complement binds to specific receptors on various cell types to mediate its inflammatory and opsonic activities. The best characterized of these receptors is CR1, which binds the opsonin fragments C3b and C4b and promotes phagocytosis and clearance of antigen-antibody complexes in combination with antibody binding to FcR.
Receptors for the anaphylatoxins signal for mast cell degranulation (releasing histamine) and smooth muscle contraction. C5a receptor also signals macrophages to phagositize complement-coated antigen in the absence of IgG binding to FcR