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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...
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| Kieli: | English |
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Blackwell Science Inc
2005
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| Linkit: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1809293/ https://ncbi.nlm.nih.gov/pubmed/15654819 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/j.1365-2249.2005.02698.x |
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pubmed-18092932007-07-12 Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent Islander, U Erlandsson, M C Chavoshi, T Jochems, C Movérare, S Nilsson, S Ohlsson, C Gustafsson, J-Å Carlsten, H Clin Exp Immunol Animal Studies 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. Blackwell Science Inc 2005-02 /pmc/articles/PMC1809293/ /pubmed/15654819 http://dx.doi.org/10.1111/j.1365-2249.2005.02698.x Text en © 2005 British Society for Immunology |
| institution |
US National Library of Medicine |
| collection |
PubMed Central |
| language |
English |
| format |
Article |
| topic |
Animal Studies |
| spellingShingle |
Animal Studies Islander, U Erlandsson, M C Chavoshi, T Jochems, C Movérare, S Nilsson, S Ohlsson, C Gustafsson, J-Å Carlsten, H Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent |
| description |
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. |
| author |
Islander, U Erlandsson, M C Chavoshi, T Jochems, C Movérare, S Nilsson, S Ohlsson, C Gustafsson, J-Å Carlsten, H |
| author_facet |
Islander, U Erlandsson, M C Chavoshi, T Jochems, C Movérare, S Nilsson, S Ohlsson, C Gustafsson, J-Å Carlsten, H |
| author_sort |
Islander, U |
| title |
Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent |
| title_short |
Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent |
| title_full |
Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent |
| title_fullStr |
Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent |
| title_full_unstemmed |
Estren-mediated inhibition of T lymphopoiesis is estrogen receptor-independent whereas its suppression of T cell-mediated inflammation is estrogen receptor-dependent |
| title_sort |
estren-mediated inhibition of t lymphopoiesis is estrogen receptor-independent whereas its suppression of t cell-mediated inflammation is estrogen receptor-dependent |
| publisher |
Blackwell Science Inc |
| publisher_facet |
Blackwell Science Inc |
| publishDate |
2005 |
| url |
https://ncbi.nlm.nih.gov/pmc/articles/PMC1809293/ https://ncbi.nlm.nih.gov/pubmed/15654819 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/j.1365-2249.2005.02698.x |
| _version_ |
1760357289118662656 |