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J. Clin. Med. 2017, 6(7), 67;

The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis

Institute of Rheumatology, Tokyo Women’s Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan
Author to whom correspondence should be addressed.
Received: 24 April 2017 / Revised: 28 June 2017 / Accepted: 2 July 2017 / Published: 10 July 2017
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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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. View Full-Text
Keywords: CD161; classic Th1; nonclassic Th1; plasticity; rheumatoid arthritis; Th17 CD161; classic Th1; nonclassic Th1; plasticity; rheumatoid arthritis; Th17

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Kotake, S.; Yago, T.; Kobashigawa, T.; Nanke, Y. The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis. J. Clin. Med. 2017, 6, 67.

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