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The complement system, also known as complement cascade, is a part of the humoral, innate immune system and enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane. [1]
Complement-dependent cytotoxicity (CDC) is an effector function of IgG and IgM antibodies.When they are bound to surface antigen on target cell (e.g. bacterial or viral infected cell), the classical complement pathway is triggered by bonding protein C1q to these antibodies, resulting in formation of a membrane attack complex (MAC) and target cell lysis.
IgM is a potent activator of the classical complement pathway, thus, AIHA involving IgM is characterized by complement-mediated opsonization and phagocytosis of RBCs as the amount of C3b deposited is sublytic. IgM also leads to phagocytosis of RBCs however, because phagocytic cells have receptors for the bound complement (rather than FcRs as in ...
[3] An example of complement dependent type II hypersensitivity is an acute hemolytic transfusion reaction following transfusion of ABO incompatible blood. [4] Preformed antibody (predominantly IgM) against donor red cell antigens not found in an individual of a particular blood group (e.g. anti-A IgM in an individual with blood group B), bind to the donor red cell surface and lead to rapid ...
Antibody-mediated complement activation leads to MAC deposition on the surface of infected cells. [1] Assembly of the MAC leads to pores that disrupt the cell membrane of target cells, leading to cell lysis and death. [2] The MAC is composed of the complement components C5b, C6, C7, C8 and several C9 molecules.
Complement factor H can inhibit the formation of the C3 convertase by competing with factor B for binding to C3b; [1] accelerate the decay of the C3 convertase; [2] and act as a cofactor for factor I-mediated cleavage of C3b. [3] Complement factor H preferentially binds to vertebrate cells (because of affinity for sialic acid residues ...
[8] Ligation of Fc receptors on the surfaces of immune effector cells can give rise to a number of responses, [9] such as degranulation (e.g., of mast cells, causing histamine liberation and subsequent urticaria), phagocytosis, release of pro-inflammatory cytokines and chemokines, platelet activation [10] resulting in the formation of clots, etc.
In human mononuclear phagocytes, phagocytosis of Mycobacterium tuberculosis is mediated in part by human monocyte complement receptors including CR3. [8] CR3 has also been shown to mediate phagocytosis of the Lyme disease causing bacterium, Borrelia burgdorferi, in the absence of iC3b opsonization. [9]