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- W4313351523 abstract "Abstract Activation of Toll-like receptors (TLRs) by pathogens triggers cytokine production and T cell activation, immune defense mechanisms that can cause immunopathology. Previous studies have established that Myd88-/- mice, which cannot signal through IL-1-family receptors and most TLRs, including TLR11, are acutely susceptible to infection with a protozoan parasite Toxoplasma gondii. Myd88-/- mice fail to activate T cells and produce IFN-γ essential for host resistance to the parasite. Using a comprehensive panel of cell type-specific MyD88-deficient mice, we show that T cell-intrinsic MyD88 signaling, rather than MyD88 activation in antigen-presenting cells, had a major role in Th1 polarization. T cell-specific elimination of MyD88 reduced IFN-γ secretion by CD4+ T cells. We also show that IFN-γ production by CD4+ Th1 cells during mucosal responses to T. gondii resulted in dysbiosis and the elimination of Paneth cells. Paneth cell death led to loss of antimicrobial peptides and occurred in conjunction with uncontrolled expansion of the Enterobacteriaceae family of Gram-negative bacteria. The expanded intestinal bacteria were responsible for the parasite-induced intestinal pathology. The investigation of cell type-specific factors regulating Th1 polarization during T. gondii infection identified the T cell-intrinsic TLR pathway as a major regulator of IFN-γ production in CD4+ T cells responsible for Paneth cell death, dysbiosis and intestinal immunopathology." @default.
- W4313351523 created "2023-01-06" @default.
- W4313351523 creator A5037972350 @default.
- W4313351523 date "2013-05-01" @default.
- W4313351523 modified "2023-10-14" @default.
- W4313351523 title "T cell-intrinsic MyD88 signaling regulates Th1 polarization and IFN-γ mediated immunopathology (P3316)" @default.
- W4313351523 doi "https://doi.org/10.4049/jimmunol.190.supp.134.11" @default.
- W4313351523 hasPublicationYear "2013" @default.
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