DefinitionThis section has been translated automatically.
Small proteins that are released from larger precursors during activation of the complement system by limited proteolysis. In a narrower sense, the cleavage products of the complement system C3a (C4a) and C5a are called anaphylatoxins (C3a and C5a have a basically similar spectrum of activity). They are wrongly named because the classical anaphylactic shock is an IgE-mediated reaction. In contrast, anaphylatoxins exert their effect directly by receptor-mediated degranulation of certain cell types. Anaphylatoxins are highly potent inflammatory mediators and trigger a variety of proinflammatory reactions on different target cells and tissues (e.g. contraction of smooth muscles, chemotaxis and degranulation of leukocytes as well as edema of the skin and mucous membranes (see below angioedema, hereditary). They are rapidly inactivated in the bloodstream by a carboxypeptidase N, which removes the C-terminal arginine residue, whereby C3a loses its activity completely, C5a loses over 90%.
LiteratureThis section has been translated automatically.
- Chazin, W J et al (1988) 1H NMR studies of human C3a anaphylatoxin in solution: sequential resonance assignments, secondary structure, and global fold. Biochemistry 27: 9139-9148
- Federwisch M. et al (1993) Tryptophan mutants of human C5a anaphylatoxin: a fluorescence anisotropy decay and energy transfer study. Biophys Chem 46: 237-248
- Markiewski MM, Lambris JD (2009) Unwelcome complement. Cancer Res 69: 6367-6770