Sex steroid receptors in peripheral T cells: absence of androgen receptors and restriction of estrogen receptors to OKT8-positive cells.

JH Cohen, L Danel, G Cordier, S Saez… - Journal of immunology …, 1983 - journals.aai.org
JH Cohen, L Danel, G Cordier, S Saez, JP Revillard
Journal of immunology (Baltimore, Md.: 1950), 1983journals.aai.org
The immune response has been reported to be modulated by sex hormones in several
models, and estrogen receptors have been demonstrated in the human thymus. We
therefore investigated the presence of estrogen and androgen receptors among human
peripheral T cells; thoracic duct lymph provided large amounts of circulating lymphocytes.
Pure T cells were obtained by negative selection by using complement-dependent
cytotoxicity with a monoclonal antibody against a monomorphic determinant of class II …
Abstract
The immune response has been reported to be modulated by sex hormones in several models, and estrogen receptors have been demonstrated in the human thymus. We therefore investigated the presence of estrogen and androgen receptors among human peripheral T cells; thoracic duct lymph provided large amounts of circulating lymphocytes. Pure T cells were obtained by negative selection by using complement-dependent cytotoxicity with a monoclonal antibody against a monomorphic determinant of class II histocompatibility antigen (HLA-DR). Furthermore, subsets of OKT8-positive and OKT8-negative lymphocytes were selected by using an OKT8-like monoclonal antibody. Sex steroid binding was determined on purified nuclei; no androgen receptors could be demonstrated on peripheral T cells. The cytoplasmic [3H] 17-beta-estradiol-receptor complex was always translocated to the nucleus in vitro within 1 hr at 37 degrees C; no estrogen receptors were demonstrable on purified OKT4-positive subsets. Assuming that estrogen receptors were evenly distributed among OKT8-positive cells, their level could be estimated to be about 40 fmol/mg DNA. The restriction of estrogen receptors to T cells bearing the "suppressor-cytotoxic" phenotype suggests a possible pathway for the modulation of T cell suppressive activities by estrogens.
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