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• W2549345201 abstract "Foxp3+ regulatory T (Treg) cells are crucial for restraining inflammation in a variety of autoimmune diseases, including type 1 diabetes (T1D). However, the transcriptional and functional phenotypes of Treg cells within the pancreatic lesion remain poorly understood. Here we characterized pancreas-infiltrating Treg cells in the NOD mouse model of T1D and uncovered a substantial enrichment of the Treg subpopulation expressing the chemokine receptor CXCR3. Accumulation of CXCR3+ Treg cells within pancreatic islets was dependent on the transcription factor T-BET, and genetic ablation of T-BET increased the onset and penetrance of disease, abrogating the sex bias normally seen in the NOD model. Both male and female mice lacking T-BET+ Treg cells showed a more aggressive insulitic infiltrate, reflected most prominently by elevated production of type 1 cytokines. Our results suggest the possibility of fine therapeutic targeting of Treg cells, in a tissue- and cell-subset-specific fashion, as a more focused immunotherapy for T1D." @default.
• W2549345201 created "2016-11-30" @default.
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• W2549345201 creator A5078237329 @default.
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• W2549345201 date "2016-11-21" @default.
• W2549345201 modified "2023-10-11" @default.
• W2549345201 title "Singular role for T-BET ⁺ CXCR3 ⁺ regulatory T cells in protection from autoimmune diabetes" @default.
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• W2549345201 doi "https://doi.org/10.1073/pnas.1616710113" @default.
• W2549345201 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5150376" @default.
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• W2549345201 hasPublicationYear "2016" @default.
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