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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.
The classical and alternative complement pathways. Complement-pathways. C3 convertase (C4bC2b, formerly C4b2a) belongs to family of serine proteases and is necessary in innate immunity as a part of the complement system which eventuate in opsonisation of particles, release of inflammatory peptides, C5 convertase formation and cell lysis.
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]
The classical and alternative complement pathways. C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the innate immune system. C3b is potent in opsonization: tagging pathogens, immune complexes (antigen-antibody), and apoptotic cells for phagocytosis.
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 ...
C5a has the highest specific biological activity and is able to act directly on neutrophils and monocytes to speed up the phagocytosis of pathogens. C3a works with C5a to activate mast cells, recruit antibody, complement and phagocytic cells and increase fluid in the tissue, all of which contribute to the initiation of the adaptive immune response.
The fragment crystallizable region (Fc region) is the tail region of an antibody that interacts with cell surface receptors called Fc receptors and some proteins of the complement system. This region allows antibodies to activate the immune system , for example, through binding to Fc receptors .
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]