Beta-endorphin modulates human immune activity via non-opiate receptor mechanisms.
Here we report that Beta-endorphin is a potent and efficacious suppressor of phytohemagglutinin induced T-lymphocyte blastogenesis when human leukocytes are exposed early in the course of mitogenic activation. This suppression becomes more difficult to observe, however, if blastogenesis is established by prior exposure to mitogen. Suppression by Beta-endorphin is not blocked by pretreatment with the opiate antagonist naloxone. These results, therefore, suggest that neuroendocrine modulation of human immune expression may be a peripheral physiological function of Beta-endorphin which is mediated by mechanisms distinct from traditional opiate receptors.
D002478:Cells, Cultured; D004723:Endorphins / Q000494:pharmacology* / Q000502:physiology; D006801:Humans; D007166:Immunosuppressive Agents; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008213:Lymphocyte Activation / Q000187:drug effects*; D009270:Naloxone / Q000494:pharmacology; D010835:Phytohemagglutinins / Q000276:immunology; D011957:Receptors, Opioid / Q000502:physiology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000201:enzymology; D001615:beta-Endorphin
D004723:Endorphins; D007166:Immunosuppressive Agents; D010835:Phytohemagglutinins; D011957:Receptors, Opioid; D009270:Naloxone; D001615:beta-Endorphin; D007770:L-Lactate Dehydrogenase