期刊
CELL REPORTS
卷 17, 期 5, 页码 1330-1343出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.09.091
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资金
- CAPES/Brazil [9693/14-09]
- Center of Gastrointestinal Biology and Disease [P30 DK034987]
- PSC partners seeking a cure
- American Gastroenterological Association Research Foundation Gut Microbiome Pilot Research Award
- Pew Charitable Trusts
Normal dynamics between microbiota and dendritic cells (DCs) support modest numbers of T cells, yet these do not cause inflammation. The DCs that induce inflammatory T cells and the signals that drive this process remain unclear. Here, we demonstrate that small intestine DCs lacking the signaling attenuator A20 induce inflammatory T cells and that the signals perceived and antigen-presenting cell (APC) functions are unique for different DC subsets. Thus, although CD103(+)CD11b(+) DCs exclusively instruct IFN gamma(+) T cells, CD103(+)CD11b(+) DCs exclusively instruct IL-17(+) T cells. Surprisingly, APC functions of both DC subsets are upregulated in a MyD88-independent fashion. In contrast, CD103(-)CD11b(+) DCs instruct both IFN gamma(+) and IL-17(+) T cells, and only the IL-17-inducing APC functions require MyD88. In disease pathogenesis, both CD103(-)CD11b(+) and CD103(+)CD11b(+) DCs expand pathologic Th17 cells. Thus, in disease pathogenesis, specific DCs instruct specific inflammatory T cells.
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