C3a (70-77) is an octapeptide corresponding to the COOH terminus of C3a, exhibits the specificity and 1 to 2% biologic activities of C3a.
The direct interaction of C3a(70-77) with human mononuclear leukocytes in culture results in a concentrationdependent inhibition of the generation of LIF evoked by mitogens and by the antigen SK-SD. The extent of suppression of LIF generation by C3a(70-77) is significant at concentrations of 10-7 M or higher and exceeds 75% at 10-6 M, irrespective of the stimulus[1]. C3a (70-77), an octapeptide corresponding to the COOH terminus of human C3a, exhibits the specificity and biologic activities of C3a. Although lacking 69 residues at the NH2 terminus, it maintains 1 to 2% of the activity of natural human C3a. C3a (70-77), Ala-Ser-HisLeu-Gly-Leu-Ala-Arg, induces histamine release and degranulation of rat mast cells, promotes contraction of guinea pig ileal tissue, and enhances vascular permeability in human skin. C3a (70-77) selectively desensitizes ileal smooth muscle to C3a but not to human C5a, a related anaphylatoxin. Conversely, C3a-(70-77) is unable to contract ileal smooth muscle pretreated with natural C3a. This cross-desensitization indicates a specific interaction of C3a (70-77) with cellular C3a binding sites[2].
[1]. Payan DG, et al. Modulation of human lymphocyte function by C3a and C3a(70-77). J Exp Med. 1982 Sep 1;156(3):756-65. [2]. Caporale LH, et al. The active site of C3a anaphylatoxin. J Biol Chem. 1980 Nov 25;255(22):10758-63.