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- W4313382108 abstract "Abstract Yersinia enterocolitica causes food-borne disease and targets the small intestine, in which ILC3 are the predominant ILC subset. Here we show that ILC3 are required for protection of mice from oral Y. enterocolitica, as mice lacking ILC3 were more susceptible and transfer of ILC to recipients was protective. IFNγ is a cytokine required for host defense from this pathogen, and while ILC in the small intestine did not increase in number they greatly increased IFNγ production after infection. The herpes virus entry mediator (HVEM), a member of the TNF receptor superfamily (TNFRSF), is expressed by all intestinal ILC subsets. Mice with a deficiency of HVEM expression in RORγt+ ILC had a reduced steady-state IL-22 production, and in vitro HVEM could signal to ILC3 to stimulate IL-22 secretion. Moreover, following oral infection with Y. enterocolitica, mice with HVEM deficiency mediated by Rorc-cre showed reduced survival and increased bacterial translocation early after infection. Cytokines are known to induce ILC activation, but our results demonstrate a novel role for the cell surface receptor HVEM in regulating ILC3 cytokine production, both at steady state, and as a critical survival factor during acute infection." @default.
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- W4313382108 date "2017-05-01" @default.
- W4313382108 modified "2023-09-26" @default.
- W4313382108 title "HVEM expression by innate lymphoid cells protects against enteric bacterial infection" @default.
- W4313382108 doi "https://doi.org/10.4049/jimmunol.198.supp.200.8" @default.
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