complement cascade


Also found in: Dictionary, Thesaurus, Medical.
Related to complement cascade: Membrane attack complex

complement cascade

[′käm·plə·mənt kas′kād]
(immunology)
The sequential activation of complement proteins resulting in lysis of a target cell.
References in periodicals archive ?
SOLIRIS (eculizumab) is a first-in-class complement inhibitor that works by inhibiting the C5 protein in the terminal part of the complement cascade, a part of the immune system.
MASP1 and MASP2 then bind to arrays of mannose groups on the surface of a bacterial cell.28 C3 and C5 are the key element of the complement cascade activation system and markers.
Figure 3(b) shows the most notable 10 of 14 REACTOME pathways, with the most common being "platelet degranulation" (8 proteins), followed by "regulation of complement cascade" (4 proteins), "integrin cell surface interactions" (4 proteins), and "amyloid fiber formation" (4 proteins).
Synapse removal is regulated, among other mechanisms, by the classical complement cascade.
lanceolatus to activate the Complement cascade in vitro, and interact with its proteins, regulators, and receptors.
C3, C5, C3a, C5a, and ASP are the major components of the complement cascade that affect metabolic reactions.
Immune complex deposition is also considered a mechanism leading to activation of the complement cascade. Antibodies associated with autoimmune hepatitis, including anti-nuclear antibody, anti-smooth muscle antibody, and peripheral anti-neutrophil cytoplasmic antibody, are involved in immune complex deposition, which may lead to activation of the complement cascade and/or promotion of T helper response.
The complement cascade functions in the immediate responses to invading microorganisms.
Clq is a member of the complement cascade, a group of immune system proteins that calls in microglial cells to gobble up synapses or cells.
It regulates the activity of the complement component C1, the first step in the classic complement cascade. Furthermore, C1INH has a regulatory role in the contact, fibrinolytic, and coagulation pathways.
Those altered to accelerate the complement cascade developed faster OA upon exposure to a physically damaging trigger.
Full browser ?