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• W2153886009 abstract "TCR signaling is important for regulatory T cell (Tr) development. Using a genetic model of DNA methyltransferase 1 (Dnmt1) deficiency, we observed highly efficient Foxp3 induction following TCR stimulation, suggesting a dominant role for TCR signaling in Foxp3 induction. In the absence of Dnmt1, Foxp3 induction in thymic and peripheral Foxp3-negative T cells was maximized upon TCR engagement, and the provision of TGF-beta was dispensable for Foxp3 expression. In addition, CD4-Cre x dnmt1(fl/fl) mice harbored sizeable thymic and peripheral populations of CD8(+)Foxp3(+) cells, suggesting that Dnmt1 activity is required for restricting Foxp3 expression to the CD4 T cell lineage. Our results suggest that the TCR signal is sufficient for transcriptional activation of Foxp3 in the absence of maintenance DNA methylation and that TGF-beta facilitates Foxp3 induction in part by opposing cell cycle-dependent Dnmt1 recruitment, leading to locus inactivation." @default.
• W2153886009 created "2016-06-24" @default.
• W2153886009 creator A5030125111 @default.
• W2153886009 creator A5033246918 @default.
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• W2153886009 date "2009-05-19" @default.
• W2153886009 modified "2023-10-03" @default.
• W2153886009 title "Cutting Edge: TCR Stimulation Is Sufficient for Induction of Foxp3 Expression in the Absence of DNA Methyltransferase 1" @default.
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• W2153886009 doi "https://doi.org/10.4049/jimmunol.0803320" @default.
• W2153886009 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19454658" @default.
• W2153886009 hasPublicationYear "2009" @default.
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