c-MAF-dependent regulatory T cells mediate immunological tolerance to a gut pathobiont

Mo Xu, Maria Pokrovskii, Yi Ding, Ren Yi, Christy Au, Oliver J. Harrison, Carolina Galan, Yasmine Belkaid, Richard Bonneau and Dan R. Littman ()
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Mo Xu: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Maria Pokrovskii: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Yi Ding: University of Rochester Medical Center
Ren Yi: Courant Institute of Mathematical Sciences, New York University
Christy Au: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Oliver J. Harrison: Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH
Carolina Galan: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine
Yasmine Belkaid: Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH
Richard Bonneau: Courant Institute of Mathematical Sciences, New York University
Dan R. Littman: Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine

Nature, 2018, vol. 554, issue 7692, 373-377

Abstract: The transcription factor c-MAF is required for the generation of Helicobacter-specific regulatory T cells that selectively restrain pro-inflammatory TH17 cells; the absence of c-MAF in mouse regulatory T cells results in pathobiont-dependent inflammatory bowel disease.

Date: 2018
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DOI: 10.1038/nature25500

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