期刊
NATURE IMMUNOLOGY
卷 15, 期 7, 页码 676-686出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2920
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资金
- Clinical Research Group CEDER of the German Research Council
- Deutsche Forschungsgemeinschaft [WE 4656/1-1]
- Interdisziplinares Zentrum fur Klinische Forschung
- Emerging Field Initiative
- ELAN programs of the University Erlangen-Nurnberg
- Deutsche Forschungsgemeinschaft Collaborative Research Centers [643, 796]
- American Asthma Foundation
- UK Medical Research Council
- Wellcome Trust [100963]
- Agency for Science Technology and Research
- MRC [MC_U105178805] Funding Source: UKRI
- Medical Research Council [MC_U105178805] Funding Source: researchfish
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 T(H)9 subset of helper T cells serves an important role in driving ulcerative colitis by regulating intestinal epithelial cells and that T(H)9 cells represent a likely target for the treatment of chronic intestinal inflammation.
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