Interleukin-31 promotes fibrosis and T helper 2 polarization in systemic sclerosis

Ai Kuzumi, Ayumi Yoshizaki (), Kazuki M. Matsuda, Hirohito Kotani, Yuta Norimatsu, Maiko Fukayama, Satoshi Ebata, Takemichi Fukasawa, Asako Yoshizaki-Ogawa, Yoshihide Asano, Kyojiro Morikawa, Yutaka Kazoe, Kazuma Mawatari, Takehiko Kitamori and Shinichi Sato ()
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Ai Kuzumi: The University of Tokyo
Ayumi Yoshizaki: The University of Tokyo
Kazuki M. Matsuda: The University of Tokyo
Hirohito Kotani: The University of Tokyo
Yuta Norimatsu: The University of Tokyo
Maiko Fukayama: The University of Tokyo
Satoshi Ebata: The University of Tokyo
Takemichi Fukasawa: The University of Tokyo
Asako Yoshizaki-Ogawa: The University of Tokyo
Yoshihide Asano: The University of Tokyo
Kyojiro Morikawa: The University of Tokyo
Yutaka Kazoe: Faculty of Science and Technology, Keio University
Kazuma Mawatari: The University of Tokyo
Takehiko Kitamori: The University of Tokyo
Shinichi Sato: The University of Tokyo

Nature Communications, 2021, vol. 12, issue 1, 1-18

Abstract: Abstract Systemic sclerosis (SSc) is a chronic multisystem disorder characterized by fibrosis and autoimmunity. Interleukin (IL)-31 has been implicated in fibrosis and T helper (Th) 2 immune responses, both of which are characteristics of SSc. The exact role of IL-31 in SSc pathogenesis is unclear. Here we show the overexpression of IL-31 and IL-31 receptor A (IL-31RA) in dermal fibroblasts (DFs) from SSc patients. We elucidate the dual role of IL-31 in SSc, where IL-31 directly promotes collagen production in DFs and indirectly enhances Th2 immune responses by increasing pro-Th2 cytokine expression in DFs. Furthermore, blockade of IL-31 with anti-IL-31RA antibody significantly ameliorates fibrosis and Th2 polarization in a mouse model of SSc. Therefore, in addition to defining IL-31 as a mediator of fibrosis and Th2 immune responses in SSc, our study provides a rationale for targeting the IL-31/IL-31RA axis in the treatment of SSc.

Date: 2021
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DOI: 10.1038/s41467-021-26099-w

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