Prolactin regulation of apoptosis-associated gene expression in T cells.
Evidence accumulated over the last two decades indicates important actions for prolactin (PRL) in regulation of several functions of the immune system. That PRL can serve to facilitate immune cell proliferation is well established. In addition, PRL appears to play a salient role in the genesis and/or potentiation of certain autoimmune diseases. Recent evidence from several laboratories has extended the spectrum of PRL actions in immunological systems to include regulation of lymphocyte pool size through the process of apoptosis. Experimental results obtained using lactogen-dependent rat pre-T cell lines, the Nb2 lymphoma, have demonstrated that PRL suppresses cell death mechanisms activated by cytokine/hormone deprivation and cytotoxic drugs such as glucocorticoids. In this paper, we review results from studies conducted to investigate the mechanism(s) underlying PRL-regulated apoptosis suppression. Effects of the hormone on expression of apoptosis-associated genes of the Bcl-2 family as well as the protooncogene pim-1 in proliferating Nb2 sublines and in cells exposed to apoptotic stimuli are presented. It is concluded that PRL-mediated apoptosis suppression in immune cells reflects a complex interaction among several gene products.
College of Pharmacy, Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, 3223 Eden Avenue, P.O. Box 670004, Cincinnati, OH 45267-0004, USA. Arthur.Buckley@uc.edu
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D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D005786:Gene Expression Regulation / Q000276:immunology*; D006801:Humans; D015213:Neuroimmunomodulation; D011388:Prolactin / Q000276:immunology*; D013601:T-Lymphocytes / Q000473:pathology* / Q000502:physiology*
D011388:Prolactin