C3a/C3a-desArg

The complement system is an important factor in innate immunity. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. An inherited deficiency of C3 predisposes the person to frequent assaults of bacterial infections. Proteolysis by certain enzymes results in the cleavage of C3 into C3a and C3b. C3a is a mediator of local inflammatory processes. C3a does induce smooth muscle contraction, increases vascular permeability, and causes histamine release from mast cells and basophilic leukocytes. C3a itself is very short-lived and in serum is cleaved rapidly into the more stable C3a-desArg (also called acylation stimulating protein, ASP) . Therefore, measurement of C3a-desArg allows reliable conclusions about the level of complement activation in the test samples.