complement cascade


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Related to complement cascade: Membrane attack complex

complement cascade

a biochemical process involving the C1 to C9 complement proteins in which one protein interacts with another in a specific sequence called a complement pathway. C5b with C6, C7, C8, and C9 form the membrane attack complex that initiates cell lysis. Other molecules, such as C3a and C5a, act as cytokines, leading to inflammation.

complement cascade

Immunology A complex, multimolecular biologic system with ± 25 different proteins that self-assemble on cell surfaces, functioning in concert with the specific immune systems to mediate host reactions and anti-microbial defense; the coup de grâce for the hapless target cell is the polymerization of C9 on its surface, which forms a transmembrane 'doughnut' that facilitates the egress of ions, cell lysis and death. See Complement. Cf Alternate pathway, Classic pathway, Common pathway.

complement

a complex series of enzymatic proteins occurring in normal serum that are triggered in a cascade manner by, and combine with, the antibody-antigen complexes, producing lysis when the antigen is an intact cell. Complement comprises 25 to 30 discrete proteins, labeled numerically as C1 to C9, and by letters, i.e. B, D, P, etc., and with C1 being divided into subcomponents C1q, C1r and C1s. Components C3 and C5 are involved in the generation of anaphylatoxin and in the promotion of leukocyte chemotaxis, the result of these two activities being the inflammatory response. C1 and C4 are involved in the neutralization of viruses. The components also combine in various sequences to participate in other biological activities, including antibody-mediated immune lysis, phagocytosis, opsonization and anaphylaxis. The complement system is known to be activated by the immunoglobulins IgM and IgG.

alternate complement pathway, alternative complement pathway
the sequence in which complement components C3 and C5 to C9 are activated without participation by C1, C2 and C4 or the presence of an antibody-antigen complex.
complement cascade
the sequence of reactions, each being the catalyst for the next, that leads to the terminal complement pathway and cell lysis. There are two pathways for activation of C3, the 'classical' (below) and the 'alternate' (above).
classical complement pathway
the one in which all of the complement components C1 to C9 participate and is triggered by antibody-antigen complexes.
complement deficiency
various complement components may be deficient without serious effects on the host. C3 deficiency is most severe and occurs in humans, Brittany spaniels and Finnish-Landrace lambs. Increased susceptibility to infections results.
complement fixation tests
utilize antibody-antigen reaction and result in hemolysis to determine the presence of various organisms in the blood. Involves two stages. In the first, also referred to as the test system, antigen is mixed usually with serial dilutions of a test serum in the presence of complement. If the serum contains antibody, i.e. is positive, an antibody-antigen complex is formed which also binds (fixes) complement. In the second stage, also called the indicator system, sheep red blood cells coated with specific, usually rabbit anti-sheep red blood cell antibody are added. The red blood cells are said to be sensitized. If antibody was not present in stage 1, then the free complement lyses the sensitized sheep red blood cells. The basis of many serological tests including those for glanders, tuberculosis and contagious bovine pleuropneumonia. Called also Bordet-Gengou phenomenon. See also immunity.
complement regulatory proteins
a set of at least seven proteins that are present in plasma (C1 INH, C4b-binding protein, factor H and factor I) or present in cell membranes (decay-accelerating factor [DAF], membrane cofactor protein [MCP] and homologous restriction factor [HHF]) that modulate the complement proteins and protect 'innocent' bystander cells and tissues from complement damage.
terminal complement pathway
the final stages of complement activation in which C5, C6, C7, C8 and C9 are activated; common to both the alternate and classical pathways.
References in periodicals archive ?
Barres has created a start-up company, called Annexon, to develop drugs to block the action of Clq and other proteins in the complement cascade.
In order to complete our research, a second test, aimed at indirectly detecting the anti-inflammatory activity, was performed on extracts impairing the complement cascade.
Investigators have recently transplanted into nonhuman primates the organs of pigs genetically engineered to avoid the complement cascade.
There are also data suggesting that microglia and/or the complement cascade may be involved in neurodevelopmental disorders such as autism, epilepsy or schizophrenia, perhaps altering the brain's normal balance of synapses.
Complement inhibitors: The Company has three products in research and development - APT070, a fragment of CR1 (complement receptor 1), which is currently in an early Phase I/II human clinical trial in rheumatoid arthritis, and, CD59 and CD55, two different complement inhibitors, which function at different sites in the complement cascade.
Due to the biochemical nature of the complement cascade, BioCryst believes complement inhibitors may have therapeutic applications in numerous acute and chronic immunological disorders.
The complement cascade refers to the precise series of events which activate each component of the complement system.
However, any of a number of stimuli including antibodies, pathogenic microorganisms, injured or normal tissue, proteases (inflammatory enzymes) and artificial surfaces can locally activate the complement cascade causing several of the circulating complement proteins to cleave into active byproducts that can cause a variety of inflammatory diseases.
Terminal complement has been linked to the destruction of red blood cells, or hemolysis, characteristic of PNH, as PNH blood cells are deficient in natural inhibitors of the complement cascade.
However, any of a number of stimuli including autoreactive antibodies, injured tissue, normal tissue, proteases (inflammatory enzymes) and artificial surfaces can locally activate the complement cascade causing several of the circulating inactive complement proteins to split and then combine with each other to form active byproducts that cause a variety of inflammatory diseases.
As Phase I of this grant, Alexion will research the role that the complement cascade plays in the viability of platelets.
Complement is a complex series of blood proteins that work in concert with antibodies; the complement cascade refers to the precise series of events which activate each component of the complement system.

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