维甲酸相关孤儿受体γt（RORγt）而非T细胞转录因子（T-bet）的过表达会加剧多发性硬化症的自身免疫模型。
RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis.
作者信息
Martinez Nicholas E, Sato Fumitaka, Omura Seiichi, Kawai Eiichiro, Takahashi Satoru, Yoh Keigyou, Tsunoda Ikuo
机构信息
Department of Microbiology and Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Department of Anatomy and Embryology, Faculty of Medicine, International Institute for Integrative Sleep Medicine (WPI-IIIS), Life Science Center, Tsukuba Research Alliance (TARA), Laboratory Animal Resource Center (LARC), University of Tsukuba, Tsukuba, Ibaraki, 305-8575, Japan.
出版信息
J Neuroimmunol. 2014 Nov 15;276(1-2):142-9. doi: 10.1016/j.jneuroim.2014.09.006. Epub 2014 Sep 16.
Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology.
辅助性T细胞17（Th17细胞）在多发性硬化症（MS）及其自身免疫模型——实验性自身免疫性脑脊髓炎（EAE）中发挥着重要作用。然而，此前的研究尚未探讨增强的Th17免疫反应如何影响脱髓鞘疾病。我们在过表达一种Th17诱导转录因子的维甲酸相关孤儿受体γt（RORγt）转基因C57BL/6小鼠中用髓鞘少突胶质细胞糖蛋白（MOG）诱导EAE。RORγt转基因小鼠比野生型小鼠发生更严重的EAE，且具有更强的抗MOG Th17免疫反应。相反，过表达一种Th1诱导转录因子——T盒转录因子（T-bet）的小鼠对EAE具有抗性。因此，偏向Th17免疫反应的遗传倾向可能导致中枢神经系统免疫病理学改变。
Zotero 插件