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- W4313386077 abstract "Abstract Polymorphisms attenuating IL-10 signaling confer genetic risk for inflammatory bowel disease. Yet how IL-10 prevents mucosal autoinflammation is incompletely understood. We demonstrate using lineage-specific deletions of IL-10Rα that IL-10 acts primarily through macrophages to limit colitis. A macrophage-selective deficiency of IL-10Rα increases the severity of colitis induced by T cell transfer into Rag1-/- mice to the same extent as germline deletion of the gene. Colitis mediated by T cell transfer is Th17 cell dependent regardless of the expression of IL-10Rα. Disease development requires IL-6 to support pathologic Th17 cell generation in wild type mice. However, specific ablation of macrophage IL-10Rα provokes excessive IL-1β production that overrides Th17 IL-6 dependence, amplifying the colonic Th17 response and disease severity. IL-10 not only inhibits pro-IL-1β production transcriptionally in macrophages, but suppresses caspase-1 activation and caspase-1 dependent maturation of pro-IL-1β to IL-1β. Therefore lineage-specific effects of IL-10 skew the cytokine dependency of Th17 development required for colitis pathogenesis. Coordinated interventions may be needed to fully suppress Th17-mediated immunopathology." @default.
- W4313386077 created "2023-01-06" @default.
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- W4313386077 date "2015-05-01" @default.
- W4313386077 modified "2023-09-27" @default.
- W4313386077 title "IL-10 engages macrophages to shift Th17 cytokine dependency and pathogenicity during T cell-mediated colitis (MUC8P.729)" @default.
- W4313386077 doi "https://doi.org/10.4049/jimmunol.194.supp.204.9" @default.
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