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Estrogen receptor alpha contributes to T cell-mediated autoimmune inflammation by promoting T cell activation and proliferation
Tekijät: Mohammad I, Starskaia I, Nagy T, Guo JT, Yatkin E, Väänänen K, Watford WT, Chen Z
Kustantaja: AMER ASSOC ADVANCEMENT SCIENCE
Julkaisuvuosi: 2018
Journal: Science Signaling
Tietokannassa oleva lehden nimi: SCIENCE SIGNALING
Lehden akronyymi: SCI SIGNAL
Artikkelin numero: ARTN eaap9415
Vuosikerta: 11
Numero: 526
Sivujen määrä: 12
ISSN: 1945-0877
eISSN: 1937-9145
DOI: https://doi.org/10.1126/scisignal.aap9415
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/Publication/31088147
Tiivistelmä
It has long been appreciated that most autoimmune disorders are characterized by increased prevalence in females, suggesting a potential role for sex hormones in the etiology of autoimmunity. To study how estrogen receptor. (ER alpha) contributes to autoimmune diseases, we generated mice in which ER alpha was deleted specifically in T lymphocytes. We found that ER alpha deletion in T cells reduced their pathogenic potential in a mouse model of colitis and correlated with transcriptomic changes that affected T cell activation. ER alpha deletion in T cells contributed to multiple aspects of T cell function, including reducing T cell activation and proliferation and increasing the expression of Foxp3, which encodes a critical transcription factor for the differentiation and function of regulatory T cells. Thus, these data demonstrate that ER alpha in T cells plays an important role in inflammation and suggest that ER alpha-targeted immunotherapies could be used to treat autoimmune disorders.
It has long been appreciated that most autoimmune disorders are characterized by increased prevalence in females, suggesting a potential role for sex hormones in the etiology of autoimmunity. To study how estrogen receptor. (ER alpha) contributes to autoimmune diseases, we generated mice in which ER alpha was deleted specifically in T lymphocytes. We found that ER alpha deletion in T cells reduced their pathogenic potential in a mouse model of colitis and correlated with transcriptomic changes that affected T cell activation. ER alpha deletion in T cells contributed to multiple aspects of T cell function, including reducing T cell activation and proliferation and increasing the expression of Foxp3, which encodes a critical transcription factor for the differentiation and function of regulatory T cells. Thus, these data demonstrate that ER alpha in T cells plays an important role in inflammation and suggest that ER alpha-targeted immunotherapies could be used to treat autoimmune disorders.
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