The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis

Shigeru Kotake; Toru Yago; Tsuyoshi Kobashigawa; Yuki Nanke

doi:10.3390/jcm6070067

The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis

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

Authors

Shigeru Kotake¹, Toru Yago², Tsuyoshi Kobashigawa³, Yuki Nanke⁴

Affiliations

¹ Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan. skotake@twmu.ac.jp.
² Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan. toruyago@gmail.com.
³ Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan. kbsgwtys@gmail.com.
⁴ Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan. ynn@twmu.ac.jp.

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.

Keywords: CD161; Th17; classic Th1; nonclassic Th1; plasticity; rheumatoid arthritis.

Publication types

Review