Modulation of the autologous mixed lymphocyte reaction by beta-endorphin.
The effect of the opiate peptide, beta-endorphin (beta-END), on the autologous and allogeneic mixed lymphocyte reaction was examined. Physiologic concentrations of beta-END augmented proliferation of the autologous mixed lymphocyte reaction (AMLR) but the allogeneic MLR was not altered. Alpha-endorphin (alpha-END) was ineffective. Pre-incubation of the stimulator subset (i.e., B cells and macrophages) with 10(-8) M beta-END followed by addition to AMLR culture without additional opiate peptide did not produce augmentation. The beta-END-induced augmentation of the AMLR was partially inhibited by the opiate antagonist naloxone. beta-END augmentation was not due to increased secretion of interleukin-2. When prostaglandin E2 (PGE2) was added to AMLR cultures wherein the stimulator cell fraction was vigorously depleted of adherent cells, suppression was observed which could be reversed by the addition of beta-END (10(-8) M). The potential mechanisms producing the increased proliferative response during the AMLR are discussed.
Froelich
C J
CJ
Department of Medicine, University of Illinois, Chicago 60612.
D000911:Antibodies, Monoclonal / Q000276:immunology; D015232:Dinoprostone; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000187:drug effects; D007959:Lymphocyte Culture Test, Mixed; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology; D011458:Prostaglandins E / Q000494:pharmacology; D011957:Receptors, Opioid / Q000502:physiology; D001615:beta-Endorphin / Q000494:pharmacology*
D000911:Antibodies, Monoclonal; D007376:Interleukin-2; D011458:Prostaglandins E; D011957:Receptors, Opioid; D001615:beta-Endorphin; D015232:Dinoprostone