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A dysbiotic microbiome triggers T<sub>H</sub>17 cells to mediate oral mucosal immunopathology in mice and humans.


ABSTRACT: Periodontitis is one of the most common human inflammatory diseases, yet the mechanisms that drive immunopathology and could be therapeutically targeted are not well defined. Here, we demonstrate an expansion of resident memory T helper 17 (TH17) cells in human periodontitis. Phenocopying humans, TH17 cells expanded in murine experimental periodontitis through local proliferation. Unlike homeostatic oral TH17 cells, which accumulate in a commensal-independent and interleukin-6 (IL-6)-dependent manner, periodontitis-associated expansion of TH17 cells was dependent on the local dysbiotic microbiome and required both IL-6 and IL-23. TH17 cells and associated neutrophil accumulation were necessary for inflammatory tissue destruction in exp

SUBMITTER: Dutzan N 

PROVIDER: S-EPMC6330016 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature