Journal
IMMUNITY
Volume 50, Issue 1, Pages 212-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2018.12.015
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Funding
- NIH (NIGMS) [GM108505]
- NIH (NCCIH) [AT008661]
- Janssen Human Microbiome Institute
- CCFA Microbiome Innovation Award [362048]
- New York Crohn's Foundation
- NIH [DK108487, DK112679, DK085691, CA016042, UL1TR000124]
- Crohn's and Colitis Foundation of America
- Cancer Center Support Grant [P30CA016087]
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Microbiota are thought to influence the development and progression of inflammatory bowel disease (IBD), but determining generalizable effects of microbiota on IBD etiology requires larger-scale functional analyses. We colonized germ-free mice with intestinal microbiotas from 30 healthy and IBD donors and determined the homeostatic intestinal T cell response to each microbiota. Compared to microbiotas from healthy donors, transfer of IBD microbiotas into germ-free mice increased numbers of intestinal Th17 cells and Th2 cells and decreased numbers of ROR gamma t(+) Treg cells. Colonization with IBD microbiotas exacerbated disease in a model where colitis is induced upon transfer of naive T cells into Rag1(-/-) mice. The proportions of Th17 and ROR gamma t(+) Treg cells induced by each microbiota were predictive of human disease status and accounted for disease severity in the Rag1(-/-) colitis model. Thus, an impact on intestinal Th17 and ROR gamma t(+) Treg cell compartments emerges as a unifying feature of IBD microbiotas, suggesting a general mechanism for microbial contribution to IBD pathogenesis.
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