Department of Neurology, Thomas Jefferson University, Ste. 300 JHN, 900 Walnut Street, Philadelphia, PA 19107, USA.
J Neuroimmune Pharmacol. 2010 Jun;5(2):189-97. doi: 10.1007/s11481-009-9188-9. Epub 2010 Jan 27.
Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune demyelinating diseases of the central nervous system (CNS). Interferon-gamma-producing Th1 and interleukin-17-producing Th17 CD4(+) T helper (Th) cells mediate disease pathogenesis in EAE and likely in MS as well. However, the relative contribution of each Th subset to autoimmune processes in the CNS remains unclear. Emerging data suggest that both Th1 and Th17 cells contribute to CNS autoimmunity, albeit through different mechanisms. A better understanding of the roles that Th1 and Th17 cells play in autoimmune inflammation will be helpful in developing new therapeutic approaches. In this review, we discuss recent findings on the roles of Th1 and Th17 cells in the pathogenesis of EAE.
多发性硬化症 (MS) 及其动物模型实验性自身免疫性脑脊髓炎 (EAE) 是中枢神经系统 (CNS) 的自身免疫性脱髓鞘疾病。产生干扰素-γ的 Th1 和产生白细胞介素-17 的 Th17 CD4(+)T 辅助 (Th) 细胞在 EAE 中以及可能在 MS 中介导疾病发病机制。然而,每个 Th 亚群对中枢神经系统自身免疫过程的相对贡献尚不清楚。新出现的数据表明,Th1 和 Th17 细胞都有助于中枢神经系统自身免疫,尽管通过不同的机制。更好地了解 Th1 和 Th17 细胞在自身免疫炎症中的作用将有助于开发新的治疗方法。在这篇综述中,我们讨论了 Th1 和 Th17 细胞在 EAE 发病机制中的作用的最新发现。