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

Ulrika Islander, M. C. Erlandsson, T. Chavoshi, C. Jochems, S. Movérare, S. Nilsson, C. Ohlsson, J. Å Gustafsson, H. Carlsten

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)210-215
Number of pages6
JournalClinical and Experimental Immunology
Volume139
Issue number2
DOIs
StatePublished - Feb 2005

Keywords

  • 17β-estradiol
  • Estren
  • Estrogen receptor
  • Knock-out mice
  • Thymus

ASJC Scopus subject areas

  • Immunology

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