| First Author | Mohammad I | Year | 2018 |
| Journal | Sci Signal | Volume | 11 |
| Issue | 526 | PubMed ID | 29666308 |
| Mgi Jnum | J:284421 | Mgi Id | MGI:6381133 |
| Doi | 10.1126/scisignal.aap9415 | Citation | Mohammad I, et al. (2018) Estrogen receptor alpha contributes to T cell-mediated autoimmune inflammation by promoting T cell activation and proliferation. Sci Signal 11(526) |
| abstractText | 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 alpha (ERalpha) contributes to autoimmune diseases, we generated mice in which ERalpha was deleted specifically in T lymphocytes. We found that ERalpha deletion in T cells reduced their pathogenic potential in a mouse model of colitis and correlated with transcriptomic changes that affected T cell activation. ERalpha 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 ERalpha in T cells plays an important role in inflammation and suggest that ERalpha-targeted immunotherapies could be used to treat autoimmune disorders. |
