Suppressive effect of retinoid on experimentalautoimmune uveoretinitis

最近的研究表明，维甲酸在体外抑制T细胞向Th1和Th17细胞的分化，而促进Foxp3^+T调节细胞的产生。我们研究了视黄酸受体激动剂、视黄酸和视黄酸受体-α/β特异性激动剂AM80在实验性自身免疫性葡萄膜视网膜炎(EAU)中是否有效，该动物模型具有许多与人类葡萄膜疾病相似的临床和组织学特征。维甲酸和AM80能有效地抑制EAU的炎症反应，主要是通过抑制Th1/Th17效应细胞的分化。此外，维甲酸/AM80处理组小鼠外周血T细胞表面IL-6受体α表达下调。AM80在效应期的治疗只能够延缓EAU的炎症。因此，维甲酸和合成的维甲酸Am80有望成为预防和治疗Th1/Th17途径介导的自身免疫性葡萄膜视网膜炎症的药物。

Recent studies have demonstrated that retinoids suppress T cell differentiation into Th1 and Th17 cells while promoting the generation of Foxp3^+ T regulatory cells in vitro. We examined whether retinoic acid receptor (RAR) agonist, retinoic acid and RAR-α/β specific agonist Am80 would be effective in experimental autoimmune uveoretinitis (EAU), an animal model that shares many clinical and histological features with human uveitic disorders. Administration of retinoic acid and Am80 was effective in suppressing inflammation in EAU, mainly by suppressing differentiation of Th1/Th17 effector cells. In addition, the expression of IL-6 receptor α on CD4^+ T cells was down-regulated in retinoic acid /Am80-treated mice. Am80 treatment during the effector phase only was capable of delaying inflammation in EAU. Thus, retinoic acid and the synthetic retinoid, Am80 appears to be a promising agent for preventing and treating autoimmune uveoretinal inflammation mediated by the Th1/Th17 pathway.