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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.
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 ...
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.
Characteristics of clinically significant alloantibodies include: immunoglobulin G antibody subclass, reactivity at body temperature, and ability to cause red blood cell agglutination in the presence of anti-human globulin (AHG) in an indirect antiglobulin test. [4] Sometimes, clinical significance of an antibody can be difficult to determine. [6]
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.
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]