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• W3095704885 abstract "CD4+Foxp3+Tregs maintain immune homeostasis, but distinct mechanisms underlying their functional heterogeneity during infections are driven by specific cytokine milieu. Here we show that MyD88 deletion in Foxp3+ cells altered their function and resulted in increased fungal burden and immunopathology during oral Candida albicans (CA) challenge. Excessive inflammation due to the absence of MyD88 in Tregs coincided with a reduction of the unique population of IL-17A expressing Foxp3+ cells (Treg17) and an increase in dysfunctional IFN-g+Foxp3+ cells (TregIFN-g) in infected mice. Failure of MyD88-/- Tregs to regulate effector CD4+ T cell functions correlated with heightened levels of IFN-g in CD4+ T cells as well as increased infiltration of inflammatory monocytes and neutrophils in oral mucosa in vivo. Mechanistically, IL-1b/MyD88 signaling was required for the activation of IRAK-4, Akt and mTOR, which led to the induction and proliferation of Treg17 cells. In the absence of IL-1 receptor signaling, Treg17 cells were reduced, but IL-6-driven expansion of TregIFN-g cells was increased. This mechanism was physiologically relevant during Candida infection in aged mice, as they exhibited IL-1 receptor/MyD88 defect in Foxp3+ cells, loss of p-mTORhighTreg17 cells and reduced levels of IL-1b in oral mucosa, which coincided with persistent tongue inflammation. Concurrent with Treg dysfunction, aging was associated with increased CD4+ T cell hyperactivation and heightened levels of IL-6 in mice and humans in oral mucosa in vivo. Taken together, our data identify IL-1b/MyD88/Treg axis as a new component that modulates inflammatory responses in oral mucosa. Also, dysregulation of this axis in an aging immune system may skew host defense towards an immunopathological response in mucosal compartments." @default.
• W3095704885 created "2020-11-09" @default.
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• W3095704885 date "2020-11-06" @default.
• W3095704885 modified "2023-10-17" @default.
• W3095704885 title "IL-1β-MyD88-mTOR Axis Promotes Immune-Protective IL-17A+Foxp3+ Cells During Mucosal Infection and Is Dysregulated With Aging" @default.
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• W3095704885 doi "https://doi.org/10.3389/fimmu.2020.595936" @default.
• W3095704885 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7677307" @default.
• W3095704885 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33240286" @default.
• W3095704885 hasPublicationYear "2020" @default.
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