IL-1 receptor antagonist-deficient mice develop autoimmune arthritis due to intrinsic activation of IL-17-producing CCR2+Vγ6+γδ T cells

• DOI: 10.1038/ncomms8464
• Publication Date: 2015-06-25T10:37:58Z
• Authors: Aoi Akitsu; Harumichi Ishigame; Shigeru Kakuta; Soo-hyun Chung; Satoshi Ikeda; Kenji Shimizu; Sachiko Kubo; Yang Liu; Masayuki Umemura; Goro Matsuzaki; Yasunobu Yoshikai; Shinobu Saijo; Yoichiro Iwakura
• Keywords: CCR2

Abstract Interleukin-17 (IL-17)-producing γδ T (γδ17) cells have been implicated in inflammatory diseases, but the underlying pathogenic mechanisms remain unclear. Here, we show that both CD4 + and γδ17 are required for development of autoimmune arthritis IL-1 receptor antagonist (IL-1Ra)-deficient mice. Specifically, activated direct T-cell infiltration by inducing CCL2 expression joints. Furthermore, IL-17 reporter mice reveal Vγ6 subset CCR2 preferentially produces inflamed Importantly, because IL-1Ra normally suppresses IL-1R on cells, IL-1Ra-deficient exhibit elevated which play a critical role them to produce IL-17. Our findings demonstrate mechanism adaptive innate immunity induce an disease coordinated manner.