BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis
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,
Hayato Takahashi,
Mahadev Rao,
Pawel Muranski,
Joseph G. Crompton,
George Punkosdy,
Davide Bedognetti,
Ena Wang,
Victoria Hoffmann,
Juan Rivera,
Francesco M. Marincola,
Atsushi Nakamura,
Vittorio Sartorelli,
Yuka Kanno,
Luca Gattinoni,
Akihiko Muto,
Kazuhiko Igarashi,
John J. O’Shea () and
Nicholas P. Restifo ()
Additional contact information
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
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
Atsushi Nakamura: Tohoku University Graduate School of Medicine, 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
Kazuhiko Igarashi: Tohoku University Graduate School of Medicine, 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)
Nature, 2013, vol. 498, issue 7455, 506-510
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.
Date: 2013
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DOI: 10.1038/nature12199
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