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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 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.
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.
Cinryze, a human plasma derived C1-esterase inhibitor, has been approved for use in 2008 for the prevention of hereditary angioedema attacks. [14] [15] Deficiency in the C1q protein of the classical complement pathway can lead to development of systemic lupus erythematosus.
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.
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]
In antibody-dependent cell-mediated cytotoxicity, the pathogen does not need to be internalised to be destroyed. ADCC requires an effector cell with the ability to eliminate pathogens through release of cytotoxic agents, most notably natural killer cells. However, macrophages, neutrophils and eosinophils are sometimes implicated. [6]