Transcription Factor IRF8 Directs a Silencing Programme for TH17 Cell Differentiation

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Transcription Factor IRF8 Directs a Silencing Programme for TH17 Cell Differentiation

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Title: Transcription Factor IRF8 Directs a Silencing Programme for TH17 Cell Differentiation
Author: Ouyang, Xinshou; Zhang, Ruihua; Yang, Jianjun; Li, Qingshan; Qin, Lihui; Liu, Jianguo; Ning, Huan; Shin, Min Sun; Gupta, Monica; Qi, Chen-Feng; Lira, Sergio A.; Morse, Herbert C.; Ozato, Keiko; Mayer, Lloyd; Xiong, Huabao; Zhu, Cheng; He, John Cijiang

Note: Order does not necessarily reflect citation order of authors.

Citation: Ouyang, Xinshou, Ruihua Zhang, Jianjun Yang, Qingshan Li, Lihui Qin, Chen Zhu, Jianguo Liu, et al. 2011. Transcription factor IRF8 directs a silencing programme for TH17 cell differentiation. Nature Communications 2: 314.
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Abstract: T\(_H\)17 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\(_H\)17 cells, the molecular mechanisms underlying the functional diversity of T\(_H\)17 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 T\(_H\)17-cell differentiation. Mice with a conventional knockout, as well as a T cell-specific deletion, of the Irf8 gene exhibited more efficient T\(_H\)17 cells. Indeed, studies of an experimental model of colitis showed that IRF8 deficiency resulted in more severe inflammation with an enhanced T\(_H\)17 phenotype. IRF8 was induced steadily and inhibited T\(_H\)17-cell differentiation during T\(_H\)17 lineage commitment at least in part through its physical interaction with RORγt. These findings define IRF8 as a novel intrinsic transcriptional inhibitor of T\(_H\)17-cell differentiation.
Published Version: doi:10.1038/ncomms1311
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3112536/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:5978716

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