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Estren‐mediated inhibition of T lymphopoiesis is estrogen receptor‐independent whereas its suppression of T cell‐mediated inflammation is estrogen receptor‐dependent

Estrogen has extensive effects on the immune system. The aim of the present experiments was to compare the effects of 17β‐estradiol (E2) and 4‐estren‐3α,17β‐diol (estren) on T lymphopoiesis and T cell‐dependent inflammation. In order to investigate the role of estrogen receptors (ER) in the effects of E2 and estren on the immune system, ER knock‐out mice lacking both ERα and ERβ (DERKO) were used. T lymphopoiesis and T cell‐dependent inflammation were studied by investigating thymus cellularity, the delayed‐type hypersensitivity (DTH) reaction, CD4+ T cells in spleen and serum levels of interleukin (IL)‐6. As expected, the presence of ERs was mandatory for all the effects of E2. In contrast, treatment with estren reduced thymus cellularity in ER knock‐out mice, indicating an effect through ER‐independent pathways. Interestingly, estren suppressed only DTH, the frequency of CD4+ T cells in spleen and serum levels of IL‐6 in wild‐type (WT) mice, but not in mice lacking ERs. Thus, our study is the first to show that estren inhibits T lymphopoiesis via ER‐independent pathways, whereas its suppressive effects on inflammation are ER‐dependent.