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In men, estrogens plus antiandrogens increased free cortisol levels in 24-h urine samples, decreased natural killer cell numbers, and slightly inhibited the mitogen-induced interferon-γ/interleukin-4 ratio, but up-regulated the expression of T1-associated chemokine receptors, CCR1, CXCR3, and CCR5.Conversely, in women, androgens slightly decreased free cortisol levels in 24-h urine samples and enhanced the mitogen-induced interferon-γ/interleukin-4 ratio and tumor necrosis factor-α production.Conversely, women compared to men, show a reduced antibody-dependent cell-mediated (10, 11) and natural killer (NK) cell cytotoxicity (12, 13).Third, binding sites for sex steroids are present (14–16), and sex steroids can be metabolized in immunocompetent cells (17–19), suggesting that sex steroids may affect leukocyte function directly.T1 cells seem to preferentially express the CC chemokine receptors, CCR1, CXCR3, and CCR5 (32–35), facilitating their selective migration into inflammatory lesions.The factors that influence chemokine receptor expression effects of cross-sex steroid hormones on the immune system.

M→F transsexuals were treated with ethinyl estradiol (100 μg/day; Lynoral, Organon, Oss, Netherlands) in combination with the antiandrogen cyproterone acetate (100 mg/day; Androcur, Schering AG, Weesp, The Netherlands).The body distribution of these T cells is directed by the differential expression on the cell membrane of distinct sets of adhesion molecules and chemokine receptors.Chemokines are chemotactic cytokines produced by a wide variety of cells to attract the relevant leukocytes to sites of infection and inflammation (30, 31).T helper cells can be divided into the reciprocally suppressive T helper type 1 (T2 immune responses are associated, on the one hand, with protective immunity against certain intracellular bacteria and viruses or parasites, respectively, and, on the other hand, with certain autoimmune diseases or allergy.