Complement (redirected from Good complements)

complement /com·ple·ment/ (kom´ple-ment) a heat-labile cascade system of at least 20 serum glycoproteins that interact to provide many of the effector functions of humoral immunity and inflammation, including vasodilation and increase of vascular permeability, facilitation of phagocyte activity, and lysis of certain foreign cells. It can be activated via either the classical or alternative complement pathways (qq.v.).

Schematic representation of the classical complement pathway. The pathway is initiated by binding of two antibody molecules to a multivalent antigen, followed by binding of complement protein C1q, and then by binding of two molecules each of C1r and C1s to C1q to form the active complex C1 (A). C4 binds to the C1q portion of C1 (B), and the esterolytic site on C1s activates C4 by splitting off C4b, which binds the antigen-antibody complex or the nearby cell surface (C). The same site on C1s then cleaves and activates C2 which has bound to C4b, yielding a C4b2a complex (C3 convertase) (D). The C3 convertase binds C3 and cleaves it to the active form C3b (E), which binds to the cell surface and to the C3 convertase to form a C4b2a3b complex (C5 convertase) (F). The late phase of complement activation begins when the C5 convertase cleaves C5 to the active form C5b (G). C5b remains at the cell surface and binds first C6 then C7 (H); the latter is hydrophobic and inserts into the plasma membrane (I), where it is joined by C8 (J). As many as 19 molecules of C9 then polymerize at C5678 to form pores in the plasma membrane (K); this final complex is called the membrane attack complex (MAC). Entry of water through the pores into the cell causes osmotic swelling and cell rupture (L).

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com·ple·ment (kmpl-mnt)

n.

A group of proteins found in normal blood serum and plasma that are activated sequentially in a cascadelike mechanism that allows them to combine with antibodies and destroy pathogenic bacteria and other foreign cells.

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Complement

One of several proteins in the blood that acts with other proteins to assist in killing bacteria.

Mentioned in: Meningococcemia

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complement (kom´plment),

n one of 11 complex, enzymatic serum proteins. In an antigen-antibody reaction, complement causes lysis. Complement is also involved in anaphylaxis and phagocytosis.

complement fixation,

n an immunologic reaction in which an antigen combines with an antibody and its complement, causing the complement factor to become inactive, or “fixed.”

complement-fixation test (C-F test),

n a serologic test in which complement fixation is detected, indicating the presence of a particular antigen. The Wassermann test for syphilis is a C-F test, used to detect amebiasis, Rocky Mountain spotted fever, try-panosomiasis, and typhus.

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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.

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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.