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Regulatory T-cell suppressor program co-opts transcription factor IRF4 to control TH2 responses

Author

Listed:
  • Ye Zheng

    (Howard Hughes Medical Institute,
    Department of Immunology,
    Present address: Department of Immunology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.)

  • Ashutosh Chaudhry

    (Howard Hughes Medical Institute,
    Department of Immunology,
    Present address: Department of Immunology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.)

  • Arnold Kas

    (Howard Hughes Medical Institute,
    Department of Immunology,)

  • Paul deRoos

    (Howard Hughes Medical Institute,
    Department of Immunology,
    Present address: Department of Immunology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.)

  • Jeong M. Kim

    (Howard Hughes Medical Institute,
    Department of Immunology,)

  • Tin-Tin Chu

    (Howard Hughes Medical Institute,
    Department of Immunology,)

  • Lynn Corcoran

    (The Walter and Eliza Hall Institute)

  • Piper Treuting

    (University of Washington, Seattle, Washington 98195, USA)

  • Ulf Klein

    (Institute for Cancer Genetics and Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA)

  • Alexander Y. Rudensky

    (Howard Hughes Medical Institute,
    Department of Immunology,
    Present address: Department of Immunology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.)

Abstract

T helper cells: IRF4 in control The X-chromosome-encoded transcription factor Foxp3 is thought to play a key role in the immune response as a regulator of the differentiation and suppressor function of regulatory T cells (Treg cells). Zheng et al. show here that regulatory T cells express the transcription factor IRF4 (interferon regulatory factor-4), which is essential for the differentiation of TH2 effector cells, and that IRF4 expression is dependent on Foxp3. IRF4 depletion in Treg cells induces TH2-driven autoimmune disease, leading the authors to suggest that IRF4 directs a module within Treg cells which selectively suppressesTH2 responses.

Suggested Citation

  • Ye Zheng & Ashutosh Chaudhry & Arnold Kas & Paul deRoos & Jeong M. Kim & Tin-Tin Chu & Lynn Corcoran & Piper Treuting & Ulf Klein & Alexander Y. Rudensky, 2009. "Regulatory T-cell suppressor program co-opts transcription factor IRF4 to control TH2 responses," Nature, Nature, vol. 458(7236), pages 351-356, March.
    • Handle: RePEc:nat:nature:v:458:y:2009:i:7236:d:10.1038_nature07674
    DOI: 10.1038/nature07674
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    Cited by:

    1. Chelisa Cardinez & Yuwei Hao & Kristy Kwong & Ainsley R. Davies & Morgan B. Downes & Nadia A. Roberts & Jason D. Price & Raquel A. Hernandez & Jessica Lovell & Rochna Chand & Zhi-Ping Feng & Anselm En, 2024. "IKK2 controls the inflammatory potential of tissue-resident regulatory T cells in a murine gain of function model," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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