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引起自身免疫性中枢神经系统疾病的细胞因子和效应 T 细胞亚群。

Cytokines and effector T cell subsets causing autoimmune CNS disease.

机构信息

Klinikum Rechts der Isar, Department of Neurology, Technical University Munich, Munich, Germany.

出版信息

FEBS Lett. 2011 Dec 1;585(23):3747-57. doi: 10.1016/j.febslet.2011.03.064. Epub 2011 Apr 6.

DOI:10.1016/j.febslet.2011.03.064
PMID:21477588
Abstract

Although experimental autoimmune encephalomyelitis (EAE) is limited in its potency to reproduce the entirety of clinical and histopathologic features of multiple sclerosis (MS), this model has been successfully used to prove that MS like autoimmunity in the CNS is orchestrated by autoantigen specific T cells. EAE was also very useful to refute the idea that IFN-γ producing T helper type 1 (Th1) cells were the sole players within the pathogenic T cell response. Rather, "new" T cell lineages such as IL-17 producing Th17 cells or IL-9 producing Th9 cells have been first discovered in the context of EAE. Here, we will summarize new concepts of early and late T cell plasticity and the cytokine network that shapes T helper cell responses and lesion development in CNS specific autoimmunity.

摘要

尽管实验性自身免疫性脑脊髓炎(EAE)在其效力方面受到限制,无法完全复制多发性硬化症(MS)的全部临床和组织病理学特征,但该模型已成功用于证明中枢神经系统自身免疫类似于 MS,是由自身抗原特异性 T 细胞所调控的。EAE 也非常有助于反驳这样一种观点,即 IFN-γ 产生的辅助性 T 细胞 1(Th1)细胞是致病性 T 细胞反应中唯一的参与者。相反,“新型”T 细胞谱系,如产生白细胞介素-17(IL-17)的 Th17 细胞或产生白细胞介素-9(IL-9)的 Th9 细胞,最初是在 EAE 背景下发现的。在这里,我们将总结早期和晚期 T 细胞可塑性的新概念,以及塑造中枢神经系统自身免疫中辅助性 T 细胞反应和病变发展的细胞因子网络。

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