Transcription factor IRF8 directs a silencing programme for TH17 cell differentiation

Xinshou Ouyang, Ruihua Zhang, Jianjun Yang, Qingshan Li, Lihui Qin, Chen Zhu, Jianguo Liu, Huan Ning, Min Sun Shin, Monica Gupta, Chen Feng Qi, John Cijiang He, Sergio A. Lira, Herbert C. Morse, Keiko Ozato, Lloyd Mayer, Huabao Xiong

Research output: Contribution to journalArticlepeer-review

103 Scopus citations

Abstract

TH17 cells are recognized as a unique subset of T helper cells that have critical roles in the pathogenesis of autoimmunity and tissue inflammation. Although RORγt is necessary for the generation of T H17 cells, the molecular mechanisms underlying the functional diversity of TH17 cells are not fully understood. Here we show that a member of interferon regulatory factor (IRF) family of transcription factors, IRF8, has a critical role in silencing TH17-cell differentiation. Mice with a conventional knockout, as well as a T cell-specific deletion, of the Irf8 gene exhibited more efficient TH17 cells. Indeed, studies of an experimental model of colitis showed that IRF8 deficiency resulted in more severe inflammation with an enhanced TH17 phenotype. IRF8 was induced steadily and inhibited TH17-cell differentiation during T H17 lineage commitment at least in part through its physical interaction with RORγt. These findings define IRF8 as a novel intrinsic transcriptional inhibitor of TH17-cell differentiation.

Original languageEnglish
Article number314
JournalNature Communications
Volume2
Issue number1
DOIs
StatePublished - 2011

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