In addition to pituitary hormones, hypothalamic-releasing hormone receptors and their effects have been documented on cells of the immune system (Tables 1.2 and 1.3). Corticotropin-releasing hormone (CRH) inhibits lymphocyte proliferation and NK cell activity (Jain et al. 1991; Smith et al. 1992). The GH-releasing hormone (GHRH) receptor has also been identified on cells of the immune system. The GHRH receptor binding sites are saturable and are found on both thymocytes and splenic lymphocytes (Guarcello, Weigent, and Blalock 1991). Other in vitro findings suggest GHRH may inhibit NK cell activity and chemotaxis and increase IFN-y secretion (Guarcello et al. 1991; Zelazowski et al. 1989). Recently, GHRH was shown to modulate IL-6 secretion from human peripheral blood mononuclear cells without any significant effect on IL-8 secretion (Siejka, Stepien, Lawnicka, Krupinski, Komorowski, and Stepien 2005). In addition, leukocytes have been shown to respond to thyrotropin-releasing hormone (TRH) treatment by producing thyrotropin (TSH) mRNA and protein (Kruger et al. 1989). Recent work has shown the presence of two receptor types for TRH on T cells. One of these appears to be the classical TRH receptor and is involved in the release of IFN from T cells (Harbour et al. 1990). TRH at very low concentrations enhances the in vitro plaque-forming cell response via production of TSH (Kruger et al. 1989). In this instance, T cells were shown to produce TSH while other studies suggest dendritic cells and monocytes may also produce biologically active TSH. Interestingly, T lymphocytes cultured with T3 and T4, but not TSH nor TRH, showed enhanced apoptosis with reduced expression of Bcl-2 protein (Wang and Klein 2001). The existence of distinct subsets of somatostatin (SOM) receptors on the Jurkat line of human leukemic T cells and U266 IgG-producing human myeloma cells has also been described (Hiruma et al. 1990). Two subsets of receptors may account for the biphasic concentration-dependent nature of the effects of SOM in some systems. Although GH and PRL have immunoenhancing capabilities, SOM has potent inhibitory effects on immune responses. SOM has been shown to significantly inhibit Molt-4 lymphoblast proliferation and phytohemagglutinin (PHA) stimulation of human T lymphocytes and nanomolar concentrations are able to inhibit the proliferation of both spleen-derived and Peyer's patch-derived lymphocytes (Stanisz et al. 1986). Other immune responses, such as superantigen-stimulated IFN secretion, endotoxin-induced leukocytosin, and colony-stimulating activity release, are also inhibited by SOM (Stanisz et al. 1986).
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