| First Author | Britton GJ | Year | 2019 |
| Journal | Immunity | Volume | 50 |
| Issue | 1 | Pages | 212-224.e4 |
| PubMed ID | 30650377 | Mgi Jnum | J:277395 |
| Mgi Id | MGI:6330918 | Doi | 10.1016/j.immuni.2018.12.015 |
| Citation | Britton GJ, et al. (2019) Microbiotas from Humans with Inflammatory Bowel Disease Alter the Balance of Gut Th17 and RORgammat(+) Regulatory T Cells and Exacerbate Colitis in Mice. Immunity 50(1):212-224.e4 |
| abstractText | 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 RORgammat(+) 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 RORgammat(+) 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 RORgammat(+) Treg cell compartments emerges as a unifying feature of IBD microbiotas, suggesting a general mechanism for microbial contribution to IBD pathogenesis. |
