BETA-ENDORPHIN STIMULATES RAT LYMPHOCYTE-T PROLIFERATION

β-Endorphin 1-31 and several structurally related peptides were tested for their ability to alter mitogen-induced T cell proliferation. Rat β-endorphin 1-31 and human β-endorphin 1-27 increased phytohemagglutinin (PHA)-induced [3H]thymidine incorporation into rat lymph node cells. However, when PHA-induced proliferation was suppressed by the inclusion of prostaglandin E1 (PGE1), human β-endorphin 1-31 and a number of structurally similar peptides, including some peptides that did not alter mitogen-induced proliferation, significantly reduced the PGE1 inhibition of PHA-stimulated T cell proliferation. Although the N-terminus of β-endorphin was necessary for potency, inclusion of the opioid antagonist naloxone together with β-endorphin 1-31 did not alter the blockage of PGE1 inhibition of PHA-induced proliferation caused by β-endorphin. The inhibition of mitogen-stimulated proliferation by either cholera toxin or forskolin, two additional compounds that like PGE1 also elevate cyclic AMP levels, was not blocked by β-endorphin. Verapamil suppression of proliferation was not modified by β-endorphin, indicating that the β-endorphin stimulatory effect was probably not due to Ca2+ influx through verapamil-sensitive Ca2+ channels. These data suggest that β-endorphin, acting through a nonopioid β-endorphin receptor, may modulate immunocompetence by stimulating T cell proliferation and by counteracting the inhibitory effects of PGE1. © 1990.