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• W2894735528 abstract "Clostridioides difficile infection (CDI) causes severe inflammatory responses at the intestinal mucosa but the immunological mechanisms underlying CDI-related immunopathology are still incompletely characterized. Here we identified for the first time that both, non-toxigenic strains as well as the hypervirulent ribotypes RT027 and RT023 of Clostridioides difficile (formerly Clostridium difficile), induced an effector phenotype in mucosal-associated invariant T (MAIT) cells. MAIT cells can directly respond to bacterial infections by recognizing MR1-presented metabolites derived from the riboflavin synthesis pathway constituting a novel class of antigens. We confirmed functional riboflavin synthesis of C. difficile and found fixed bacteria capable of activating primary human MAIT cells in a dose-dependent manner. C. difficile-activated MAIT cells showed an increased and MR1-dependent expression of CD69, proinflammatory IFNγ, and the lytic granule components granzyme B and perforin. Effector protein expression was accompanied by the release of lytic granules, which, in contrast to other effector functions, was mainly induced by IL-12 and IL-18. Notably, this study revealed hypervirulent C. difficile strains to be most competent in provoking MAIT cell responses suggesting MAIT cell activation to be instrumental for the immunopathology observed in C. difficile-associated colitis. In conclusion, we provide first evidence for a link between C. difficile metabolism and innate T cell-mediated immunity in humans." @default.
• W2894735528 created "2018-10-12" @default.
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• W2894735528 date "2018-10-25" @default.
• W2894735528 modified "2023-10-11" @default.
• W2894735528 title "Clostridioides difficile Activates Human Mucosal-Associated Invariant T Cells" @default.
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• W2894735528 doi "https://doi.org/10.3389/fmicb.2018.02532" @default.
• W2894735528 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6209678" @default.
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• W2894735528 hasPublicationYear "2018" @default.
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