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Nat Immunol. 2014 Jul;15(7):676-86. doi: 10.1038/ni.2920. Epub 2014 Jun 8.

TH9 cells that express the transcription factor PU.1 drive T cell-mediated colitis via IL-9 receptor signaling in intestinal epithelial cells.

Author information

1
Department of Medicine 1, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.
2
MRC Laboratory of Molecular Biology, Cambridge, UK.
3
Institute of Molecular Medicine, University Medical Center Mainz, Mainz, Germany.
4
Institute of Pathology, Campus Bodensee, Friedrichshafen, Germany.
5
Institute of Pathology, Bayreuth Clinic, Bayreuth, Germany.
6
Laboratory of Molecular Stem Cell Biology, University of Münster, Münster, Germany.
7
1] Department of Medicine 1, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany. [2].

Erratum in

  • Nat Immunol. 2015 Feb;16(2):214.

Abstract

The molecular checkpoints that drive inflammatory bowel diseases are incompletely understood. Here we found more T cells expressing the transcription factor PU.1 and interleukin 9 (IL-9) in patients with ulcerative colitis. In an animal model, citrine reporter mice had more IL-9-expressing mucosal T cells in experimental oxazolone-induced colitis. IL-9 deficiency suppressed acute and chronic colitis. Mice with PU.1 deficiency in T cells were protected from colitis, whereas treatment with antibody to IL-9 suppressed colitis. Functionally, IL-9 impaired intestinal barrier function and prevented mucosal wound healing in vivo. Thus, our findings suggest that the TH9 subset of helper T cells serves an important role in driving ulcerative colitis by regulating intestinal epithelial cells and that TH9 cells represent a likely target for the treatment of chronic intestinal inflammation.

Comment in

PMID:
24908389
DOI:
10.1038/ni.2920
[Indexed for MEDLINE]

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