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 CD103CD11b DCs exclusively instruct IFNγ T cells, CD103CD11b DCs exclusively instruct IL-17 T cells. Surprisingly, APC functions of both DC subsets are upregulated in a MyD88-independent fashion. In contrast, CD103CD11b DCs instruct both IFNγ and IL-17 T cells, and only the IL-17-inducing APC functions require MyD88. In disease pathogenesis, both CD103CD11b and CD103CD11b DCs expand pathologic Th17 cells. Thus, in disease pathogenesis, specific DCs instruct specific inflammatory T cells.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5123685PMC
http://dx.doi.org/10.1016/j.celrep.2016.09.091DOI Listing

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