anafylatoxinen

Anaphylatoxins are small peptide mediators of the complement system, produced during activation of the classical, lectin, or alternative pathways. The principal anaphylatoxins are C3a, C4a, and C5a. They are generated when the complement components C3, C4, and C5 are cleaved into active fragments (for example, C3 → C3a + C3b; C5 → C5a + C5b). These peptides exert pro-inflammatory effects by binding to specific receptors on various cells: C3a to C3a receptor (C3aR); C5a to C5a receptor 1 (C5aR1/CD88) and to a lesser extent C5aR2 (GPR77); C4a's receptor is less well defined and its effects are comparatively weaker.

The main actions of anaphylatoxins include vasodilation and increased vascular permeability, which promote edema; chemotaxis and activation of leukocytes, particularly neutrophils; and degranulation of mast cells and basophils with release of histamine and other mediators. Together these effects recruit immune cells to sites of infection or injury and amplify inflammatory responses. Anaphylatoxins are rapidly inactivated by carboxypeptidases to des-Arg forms (C3a-desArg, C4a-desArg, C5a-desArg) with reduced activity.

Clinical relevance extends to inflammatory and immune-mediated conditions. Excessive anaphylatoxin activity can contribute to tissue injury in sepsis, autoimmune diseases, allergic reactions, and ischemia-reperfusion injury. Therapeutic approaches include inhibitors of complement activation (such as C5 inhibitors) and antagonists of C5a receptors, which are used or investigated to mitigate inflammatory damage in various diseases.