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BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis

Author

Listed:
  • Rahul Roychoudhuri

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Kiyoshi Hirahara

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA
    Present address: Department of Advanced Allergology of the Airway, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.)

  • Kambiz Mousavi

    (Laboratory of Muscle Stem Cells and Gene Regulation, NIAMS, NIH, Bethesda, Maryland 20892, USA)

  • David Clever

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Christopher A. Klebanoff

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Michael Bonelli

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA)

  • Giuseppe Sciumè

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA)

  • Hossein Zare

    (Laboratory of Muscle Stem Cells and Gene Regulation, NIAMS, NIH, Bethesda, Maryland 20892, USA)

  • Golnaz Vahedi

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA)

  • Barbara Dema

    (Laboratory of Molecular Immunogenetics, NIAMS, NIH, Bethesda, Maryland 20892, USA)

  • Zhiya Yu

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Hui Liu

    (NIH)

  • Hayato Takahashi

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA)

  • Mahadev Rao

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Pawel Muranski

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Joseph G. Crompton

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • George Punkosdy

    (National Institutes of Allergy and Infectious Diseases, NIH)

  • Davide Bedognetti

    (NIH)

  • Ena Wang

    (NIH)

  • Victoria Hoffmann

    (NIH)

  • Juan Rivera

    (Laboratory of Molecular Immunogenetics, NIAMS, NIH, Bethesda, Maryland 20892, USA)

  • Francesco M. Marincola

    (NIH
    Sidra Medical and Research Centre)

  • Atsushi Nakamura

    (Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan
    CREST, Japan Science and Technology Agency, Sendai 980-8575, Japan)

  • Vittorio Sartorelli

    (Laboratory of Muscle Stem Cells and Gene Regulation, NIAMS, NIH, Bethesda, Maryland 20892, USA)

  • Yuka Kanno

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA)

  • Luca Gattinoni

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH))

  • Akihiko Muto

    (Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan
    CREST, Japan Science and Technology Agency, Sendai 980-8575, Japan)

  • Kazuhiko Igarashi

    (Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan
    CREST, Japan Science and Technology Agency, Sendai 980-8575, Japan)

  • John J. O’Shea

    (Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, Bethesda, Maryland 20892, USA)

  • Nicholas P. Restifo

    (Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH)
    NIH Center for Regenerative Medicine, NIH)

Abstract

Diverse autoimmune and allergic diseases are associated with polymorphisms in a locus encoding the transcription factor BACH2; here, BACH2 is shown to be a broad regulator of immune activation that stabilizes the differentiation of Treg cells by repressing commitment of CD4+ T cells to alternate cell fates.

Suggested Citation

  • Rahul Roychoudhuri & Kiyoshi Hirahara & Kambiz Mousavi & David Clever & Christopher A. Klebanoff & Michael Bonelli & Giuseppe Sciumè & Hossein Zare & Golnaz Vahedi & Barbara Dema & Zhiya Yu & Hui Liu , 2013. "BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis," Nature, Nature, vol. 498(7455), pages 506-510, June.
    • Handle: RePEc:nat:nature:v:498:y:2013:i:7455:d:10.1038_nature12199
    DOI: 10.1038/nature12199
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