抑制炎症反应的实验性关节炎是通过雌激素受体α但不是雌激素受体β介导。
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Dulos J, Vijn P C·多尔恩,霍夫斯特拉CL, Veening-Griffioen D,格拉夫J, Dijcks FA、靴子
抑制炎症反应的实验性关节炎是通过雌激素受体α但不是雌激素受体β介导。
关节炎Res其他。2010;12 (3):R101。doi: 10.1186 / ar3032。2010年5月24日Epub。
- PubMed ID
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20497523 (在PubMed]
- 文摘
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作品简介:免疫调节雌激素在炎症中的作用是复杂的。赞成和描述了雌激素的抗炎作用。雌激素与雌激素受体(ER)α和β。ERalpha的贡献和ERbeta ER-mediated免疫调制研究延迟型超敏反应(DTH)在实验性关节炎方法:ER-mediated抑制大鼠佐剂关节炎(AA)研究了使用乙炔雌二醇(EE)和选择性ERbeta受体激动剂(erb - 79)。关节炎后2周。接下来,影响ER受体激动剂(炔雌醇,ERalpha选择性受体激动剂(时代- 63)和选择性ERbeta受体激动剂(erb - 79)开发的破伤风类毒素(TT)您延迟类型野生型超敏反应(WT)和ERalpha——或者ERbeta-deficient老鼠了。最后,EE和时代- 63检测其免疫调节潜力建立DBA / 1 j小鼠胶原诱导关节炎。关节炎后三个星期。联合了病理组织学和放射学。当地的滑膜细胞因子的生产使用Luminex技术进行了分析。 Sera were assessed for COMP as a biomarker of cartilage destruction. RESULTS: EE was found to suppress clinical signs and symptoms in rat AA. The selective ERbeta agonist ERB-79 had no effect on arthritis symptoms in this model. In the TT-specific DTH model, EE and the selective ERalpha agonist ERA-63 suppressed the TT-specific swelling response in WT and ERbetaKO mice but not in ERalphaKO mice. As seen in the AA model, the selective ERbeta agonist ERB-79 did not suppress inflammation. Treatment with EE or ERA-63 suppressed clinical signs in collagen induced arthritis (CIA) in WT mice. This was associated with reduced inflammatory infiltrates and decreased levels of proinflammatory cytokines in CIA joints. CONCLUSIONS: ERalpha, but not ERbeta, is key in ER-mediated suppression of experimental arthritis. It remains to be investigated how these findings translate to human autoimmune disease.