In vitro potentiation of lymphocyte activation by dehydroepiandrosterone, androstenediol, and androstenetriol. Export

@article{citeulike:4298804, abstract = {Dehydroepiandrosterone (5-androstene-3 beta-ol-17-one, DHEA) has been shown to protect mice from lethal viral and bacterial infections. However, recently, androstenediol (5-androstene-3 beta-17 beta-diol, AED) and androstenetriol (5-androstene-3 beta-7 beta-triol, AET), metabolites of DHEA, have each shown to be more potent endocrine regulators of the immune response. In contrast to glucocorticosteroids, in vivo, these steroid hormones up-regulated the cellular immune response of the host to limit virus-mediated pathology. These experiments first examined the in vitro influences of DHEA, and AED, or AET on mitogen-stimulated activation of murine lymphocytes. From physiologic to pharmacologic doses, DHEA suppressed proliferation of mixed splenocyte cultures activated with Con A or LPS by 20 to 70\% whereas AED had little influence on the response. In sharp contrast, AET potentiated the response with both mitogens to 50 to 70\% above control. Analogous to these observations was the regulation of IL-2 and IL-3 secretion from Con A-activated lymphocytes by each of these hormones which again was depressed analyzed. The suppressive effects of hydrocortisone on Con A-induced lymphocyte proliferation and cytokine production were strongly counteracted by coculture with AET. DHEA did not counteract hydrocortisone activity whereas AED showed moderate antiglucocorticoid function.}, author = {Padgett, D. A. and Loria, R. M.}, citeulike-article-id = {4298804}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/8046232}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=8046232}, citeulike-linkout-2 = {http://scholar.google.com/scholar?cluster=8450722176856067602}, citeulike-linkout-3 = {http://www.jimmunol.org/cgi/content/abstract/153/4/1544}, day = {15}, issn = {0022-1767}, journal = {Journal of immunology (Baltimore, Md. : 1950)}, keywords = {aet, anti-gc, dhea\_analog}, month = {August}, number = {4}, pages = {1544--1552}, posted-at = {2009-04-10 21:15:14}, priority = {2}, title = {In vitro potentiation of lymphocyte activation by dehydroepiandrosterone, androstenediol, and androstenetriol.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/8046232}, volume = {153}, year = {1994} }

TY - JOUR ID - citeulike:4298804 L3 - citeulike-article-id:4298804 N2 - Dehydroepiandrosterone (5-androstene-3 beta-ol-17-one, DHEA) has been shown to protect mice from lethal viral and bacterial infections. However, recently, androstenediol (5-androstene-3 beta-17 beta-diol, AED) and androstenetriol (5-androstene-3 beta-7 beta-triol, AET), metabolites of DHEA, have each shown to be more potent endocrine regulators of the immune response. In contrast to glucocorticosteroids, in vivo, these steroid hormones up-regulated the cellular immune response of the host to limit virus-mediated pathology. These experiments first examined the in vitro influences of DHEA, and AED, or AET on mitogen-stimulated activation of murine lymphocytes. From physiologic to pharmacologic doses, DHEA suppressed proliferation of mixed splenocyte cultures activated with Con A or LPS by 20 to 70% whereas AED had little influence on the response. In sharp contrast, AET potentiated the response with both mitogens to 50 to 70% above control. Analogous to these observations was the regulation of IL-2 and IL-3 secretion from Con A-activated lymphocytes by each of these hormones which again was depressed analyzed. The suppressive effects of hydrocortisone on Con A-induced lymphocyte proliferation and cytokine production were strongly counteracted by coculture with AET. DHEA did not counteract hydrocortisone activity whereas AED showed moderate antiglucocorticoid function. IS - 4 JF - Journal of immunology (Baltimore, Md. : 1950) SN - 0022-1767 EP - 1552 TI - In vitro potentiation of lymphocyte activation by dehydroepiandrosterone, androstenediol, and androstenetriol. VL - 153 SP - 1544 KW - aet KW - anti-gc KW - dhea_analog AU - Padgett, DA AU - Loria, RM PY - 1994/08/15/ UR - http://view.ncbi.nlm.nih.gov/pubmed/8046232 ER -