Elsevier

Journal of Neuroimmunology

Volume 29, Issues 1–3, September–October 1990, Pages 239-248
Journal of Neuroimmunology

β-Endorphin stimulates rat T lymphocyte proliferation

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Abstract

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.

Keywords

β-Endorphin
T cell proliferation
Prostaglandin, β-Endorphin receptor
Neuroimmunomodulation

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Present address: Department of Pharmacology, Yale University, School of Medicine, New Haven, CT 06510, U.S.A.