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Th17细胞在类风湿关节炎发病机制中的可塑性

The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis.

作者信息

Kotake Shigeru, Yago Toru, Kobashigawa Tsuyoshi, Nanke Yuki

机构信息

Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan.

出版信息

J Clin Med. 2017 Jul 10;6(7):67. doi: 10.3390/jcm6070067.

Abstract

Helper T (Th) cells play an important role in the pathogenesis of autoimmune diseases, including rheumatoid arthritis (RA). It has been revealed that Th17 cells can shift to Th1 cells (i.e., "nonclassic Th1 cells"), which are reported to be more pathogenic than Th17 cells per se Thus, the association of Th cells in the pathogenesis of autoimmune disease has become more complicated. We recently reported using peripheral blood from untreated and early-onset RA patients that the ratio of CD161+Th1 cells (i.e., Th17-derived Th1 cells to CD161+Th17 cells) is elevated and that levels of interferon-γ (IFNγ)+Th17 cells are inversely correlated with levels of anti-CCP antibodies. Here, we review the plasticity of Th17 cells in the pathogenesis of RA, suggesting possible implications for novel therapies.

摘要

辅助性T(Th)细胞在包括类风湿关节炎(RA)在内的自身免疫性疾病发病机制中起重要作用。研究表明,Th17细胞可转变为Th1细胞(即“非经典Th1细胞”),据报道,非经典Th1细胞比Th17细胞本身更具致病性。因此,Th细胞在自身免疫性疾病发病机制中的关联变得更加复杂。我们最近报道,使用未经治疗的早发性RA患者的外周血发现,CD161 + Th1细胞(即Th17衍生的Th1细胞与CD161 + Th17细胞)的比例升高,且干扰素-γ(IFNγ)+ Th17细胞水平与抗环瓜氨酸肽(CCP)抗体水平呈负相关。在此,我们综述了Th17细胞在RA发病机制中的可塑性,提示其对新疗法可能具有的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df2d/5532575/b743546a0a4e/jcm-06-00067-g001.jpg

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