RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation | Zendy

Mingming Sun | Zendy; Chong He | Zendy; Liang Chen | Zendy; Wenjing Yang | Zendy; Wei Wu | Zendy; Feidi Chen | Zendy; Anthony Cao | Zendy; Suxia Yao | Zendy; Sara M. Dann | Zendy; T. G. Murali Dhar | Zendy; Luisa Salter–Cid | Zendy; Qihong Zhao | Zendy; Zhanju Liu | Zendy; Yingzi Cong | Zendy

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RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation

Author(s) -

Mingming Sun,

Chong He,

Liang Chen,

Wenjing Yang,

Wei Wu,

Feidi Chen,

Anthony Cao,

Suxia Yao,

Sara M. Dann,

T. G. Murali Dhar,

Luisa Salter–Cid,

Qihong Zhao,

Zhanju Liu,

Yingzi Cong

Publication year - 2018

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1701697

Subject(s) - rar related orphan receptor gamma , orphan receptor , microbiology and biotechnology , interleukin 17 , cellular differentiation , cell , biology , chemistry , inflammation , immunology , foxp3 , transcription factor , immune system , biochemistry , gene

The role of retinoid-related orphan receptor γ t (RORγt) in Th17 cell differentiation has been well established; however, how it regulates other T cell lineages is still not clearly understood. In this study, we report that in mice, while promoting Th17 cell differentiation, RORγt inhibited IL-10 production by T cells, thereby preserving the pathogenicity of Th17 cells. Treatment with RORγ t -specific inhibitor suppressed Th17 cell signature cytokines, but promoted IL-10 production. RORγt inhibitor-treated Th17 cells induce less severe colitis compared with control Th17 cells. Mechanistically, the RORγt inhibitor induced T cell expression of Blimp-1 (encoded by Prdm1). Prdm1 -/- T cells produced significantly fewer IL-10 when treated with RORγt inhibitor compared with wild-type T cells. Furthermore, RORγt inhibitor-treated Prdm1 -/- Th17 cells induce more severe colitis compared with RORγt inhibitor-treated wild-type Th17 cells. Collectively, our studies reveal a novel mechanism by which RORγt drives and maintains pathogenic Th17 cell development by inhibiting IL-10 production.

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