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 and Huabao Xiong ()
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Xinshou Ouyang: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Ruihua Zhang: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Jianjun Yang: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Qingshan Li: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Lihui Qin: Mount Sinai School of Medicine
Chen Zhu: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School
Jianguo Liu: Saint Louis University School of Medicine
Huan Ning: Saint Louis University School of Medicine
Min Sun Shin: Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases
Monica Gupta: Program in Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health
Chen-Feng Qi: Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases
John Cijiang He: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Sergio A. Lira: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Herbert C. Morse: Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases
Keiko Ozato: Program in Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health
Lloyd Mayer: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place
Huabao Xiong: Immunology Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place

Nature Communications, 2011, vol. 2, issue 1, 1-12

Abstract: 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 TH17 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 TH17 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.

Date: 2011
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DOI: 10.1038/ncomms1311

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