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Science. 2015 Aug 28;349(6251):993-7. doi: 10.1126/science.aaa9420. Epub 2015 Aug 13.

MUCOSAL IMMUNOLOGY. Individual intestinal symbionts induce a distinct population of RORγ⁺ regulatory T cells.

Author information

  • 1Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston 02115, MA, USA.
  • 2Division of Gastroenterology and Hepatology, Brigham and Women's Hospital, Boston, MA 02115, USA, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
  • 3Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • 4Tempero Pharmaceuticals, a GSK Company, Cambridge, MA 02115, USA.
  • 5UCB Pharma, Slough, Berkshire, UK.
  • 6Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston 02115, MA, USA. Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA. cbdm@hms.harvard.edu.

Abstract

T regulatory cells that express the transcription factor Foxp3 (Foxp3(+) T(regs)) promote tissue homeostasis in several settings. We now report that symbiotic members of the human gut microbiota induce a distinct T(reg) population in the mouse colon, which constrains immuno-inflammatory responses. This induction—which we find to map to a broad, but specific, array of individual bacterial species—requires the transcription factor Rorγ, paradoxically, in that Rorγ is thought to antagonize FoxP3 and to promote T helper 17 (T(H)17) cell differentiation. Rorγ's transcriptional footprint differs in colonic T(regs) and T(H)17 cells and controls important effector molecules. Rorγ, and the T(regs) that express it, contribute substantially to regulating colonic T(H)1/T(H)17 inflammation. Thus, the marked context-specificity of Rorγ results in very different outcomes even in closely related cell types.

Copyright © 2015, American Association for the Advancement of Science.

PMID:
26272906
[PubMed - indexed for MEDLINE]
PMCID:
PMC4700932
Free PMC Article
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