University of Muenster, Clinic for Neurology-Inflammatory Disorders of the Nervous System and Neurooncology, Muenster, Germany.
FEBS Lett. 2011 Dec 1;585(23):3764-9. doi: 10.1016/j.febslet.2011.06.027. Epub 2011 Jul 7.
IL-17 producing T helper (T(H)17) cells have recently been identified as a new subset involved in the pathogenesis of various autoimmune diseases. Exogenous factors promoting T(H)17 induction have been intensely characterized, whereas the T cell-intrinsic mechanisms influencing T(H)17 development are less established. The transcription factor RORγt, which belongs to the nuclear receptor superfamily, serves as master transcription factor essential for T(H)17 differentiation, whereas other members of the nuclear receptor family control T(H)17 differentiation and contribute to protection from T(H)17-mediated autoimmunity. In this review, we will highlight the most recent understandings about the regulatory function of nuclear receptors during T(H)17 cell differentiation.
白细胞介素-17 产生的辅助性 T 细胞(T(H)17)最近被确定为参与各种自身免疫性疾病发病机制的一个新亚群。促进 T(H)17 诱导的外源因素已得到深入研究,而影响 T(H)17 发育的 T 细胞内在机制则尚未确定。属于核受体超家族的转录因子 RORγt 作为 T(H)17 分化所必需的主转录因子,而核受体家族的其他成员控制 T(H)17 分化并有助于防止 T(H)17 介导的自身免疫。在这篇综述中,我们将重点介绍核受体在 T(H)17 细胞分化过程中的调节功能的最新认识。