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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. 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.
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. 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.
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 ...
Membrane attack complex (Terminal complement complex C5b-9) A membrane attack complex attached to a pathogenic cell The membrane attack complex (MAC) or terminal complement complex (TCC) is a complex of proteins typically formed on the surface of pathogen cell membranes as a result of the activation of the host's complement system, and as such is an effector of the immune system.
Complement component receptors CR2, CR3 and CR4 have been found to mediate this Complement-mediated enhancement of infection. [50] [52] The infection of HIV-1 leads to activation of complements. Fragments of these complements can assist viruses with infection by facilitating viral interactions with host cells that express complement receptors. [53]
After an antigen-antibody reaction, the immune complexes can be subject to any of a number of responses, including complement deposition, opsonization, [2] phagocytosis, or processing by proteases. Red blood cells carrying CR1 -receptors on their surface may bind C3b -coated immune complexes and transport them to phagocytes , mostly in liver ...