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Transcription factor IRF8 directs a silencing programme for TH17 cell differentiation

Author

Listed:
  • 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)

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.

Suggested Citation

  • 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., 2011. "Transcription factor IRF8 directs a silencing programme for TH17 cell differentiation," Nature Communications, Nature, vol. 2(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1311
    DOI: 10.1038/ncomms1311
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    Cited by:

    1. Wei-Wei Luo & Zhen Tong & Pan Cao & Fu-Bing Wang & Ying Liu & Zhou-Qin Zheng & Su-Yun Wang & Shu Li & Yan-Yi Wang, 2022. "Transcription-independent regulation of STING activation and innate immune responses by IRF8 in monocytes," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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