This review deals with the biologic actions of the complement peptides C3a, C4a, C5a, and their w-desArg derivatives. Other complementderived split products such as C2b or Ba will not be discussed. Historically, at the beginning of this century the first complement peptide was detected in immune complex-treated serum from guinea pigs. It was called" anaphylatoxin" since it produced anaphylactic shocklike symptoms after systemic application in the same animal species and was therefore regarded as the mediator of anaphylaxis (Friedberger 1910). This classical anaphylatoxin has recently been identified as C5adesArg in the porcine system (Zimmermann et aI. 1980; Gerard and Hugli 1981). Generation of further peptides from the third, fourth, and fifth components of complement (C3, C4, C5) was elucidated about 50 years later (Osler et al. 1959; Jensen t967; Cochrane and Maller-Eberhard 1968; Lepow et al. 1969). Since then a wide array of biological actions has been characterized forming a mosaic-like pattern of growing knowledge, which still has to be completed in many aspects. Complement peptides are generated in body fluids during cascading activations via two trigger pathways, the classical or the laternative, of the complement system which is a humoral defense system consisting of about 20 different proteins. In addition, they can be cleaved off selectively from their parent components by certain proteases (reviewed by Vogt 1974, 1986; Hugli and Maller-Eberhard 1978). Assuming complete conversion of the precursors maximally attainable concentrations in blood fluids of different mammalian species are 5-8Ũ 10-6 for C3 peptides, about 2Ũ t0-6 M for C4 peptides and 3-5Ũ 10-7 M for C5 peptides. By comparison, only about 20% can be reached in human lymph fluid (Vogt et al. 1986).

In general, the peptides are formed locally after unspecific or specific immunologic tissue damage and act in their proximity. Therefore, they can be regarded as autacoids or local hormones. Functionally, they are inflammatory mediators, since they activate white blood cells, smooth muscle cells, basophils/mast cells, platelets, and endothelial cells. They are involved particularly in acute inflammatory processes by their effects on unspecific defense cells, in contrast to biogenic amines (histamine, serotonin) and prostanoids which act mainly on the vascular system. According to present knowledge, the peptides initiate activation of cells by binding to specific cellular receptors. However, receptors have not yet been shown on all target cells, such as on endothelial cells, and on the target cells for their spasmogenic action in different smooth muscle organs. Recently the C5a receptor with an apparent mol. wt. of