Modulation of the autologous mixed lymphocyte reaction by β-endorphin

Abstract

The effect of the opiate peptide, β-endorphin (β-END), on the autologous and allogeneic mixed lymphocyte reaction was examined. Physiologic concentrations of β-END augmented proliferation of the autologous mixed lymphocyte reaction (AMLR) but the allogeneic MLR was not altered. Alpha-endorphin (α-END) was ineffective. Pre-incubation of the stimulator subset (i.e., B cells and macrophages) with 10 −8 M β-END followed by addition to AMLR culture without additional opiate peptide did not produce augmentation. The β-END-induced augmentation of the AMLR was partially inhibited by the opiate antagonist naloxone. β-END augmentation was not due to increased secretion of interleukin-2. When prostaglandin E 2 (PGE 2) 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 β-END (10 −8 M). The potential mechanisms producing the increased proliferative response during the AMLR are discussed.