The role of prostaglandins in C3a-mediated suppression of human in vitro polyclonal antibody responses.
Suppression of polyclonal antibody responses in human peripheral blood mononuclear cell cultures by human C3a appears to involve the release of endogenous prostaglandins from monocytes. C3a was found, under the experimental conditions employed, to activate the cyclooxygenase pathway of arachidonic acid metabolism with the release of large amounts of the prostaglandin E2 species. Suppression of the protein A-induced polyclonal antibody response by C3a is abrogated by the prostaglandin synthesis inhibitor indomethacin. In addition, physiologic amounts of exogenous PGE2 were able to inhibit polyclonal antibody secretion in a manner similar to the suppression observed when C3a was added to culture. These results suggest that C3a-induced release of prostaglandins could be a major element in immunosuppression induced by C3a.
D000917:Antibody Formation / Q000187:drug effects*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D003176:Complement C3 / Q000494:pharmacology*; D015926:Complement C3a; D016861:Cyclooxygenase Inhibitors; D003864:Depression, Chemical; D015232:Dinoprostone; D006801:Humans; D007108:Immune Tolerance; D007213:Indomethacin / Q000494:pharmacology; D009000:Monocytes / Q000378:metabolism; D011458:Prostaglandins E / Q000494:pharmacology / Q000502:physiology*
D001095:Arachidonic Acids; D003176:Complement C3; D016861:Cyclooxygenase Inhibitors; D011458:Prostaglandins E; D016718:Arachidonic Acid; D015926:Complement C3a; D015232:Dinoprostone; D007213:Indomethacin