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- W2552807099 abstract "TET proteins regulate 5-methylcytosine epigenetic marks, and thereby regulate chromatin accessibility. Rao and colleagues show that the combined loss of TET2 and TET3 in thymocytes skews development to iNKT17 cells as a result of upregulation of RORγt, which leads to lymphoproliferative disease and premature death. TET proteins oxidize 5-methylcytosine in DNA to 5-hydroxymethylcytosine and other oxidation products. We found that simultaneous deletion of Tet2 and Tet3 in mouse CD4+CD8+ double-positive thymocytes resulted in dysregulated development and proliferation of invariant natural killer T cells (iNKT cells). Tet2-Tet3 double-knockout (DKO) iNKT cells displayed pronounced skewing toward the NKT17 lineage, with increased DNA methylation and impaired expression of genes encoding the key lineage-specifying factors T-bet and ThPOK. Transfer of purified Tet2-Tet3 DKO iNKT cells into immunocompetent recipient mice resulted in an uncontrolled expansion that was dependent on the nonclassical major histocompatibility complex (MHC) protein CD1d, which presents lipid antigens to iNKT cells. Our data indicate that TET proteins regulate iNKT cell fate by ensuring their proper development and maturation and by suppressing aberrant proliferation mediated by the T cell antigen receptor (TCR)." @default.
- W2552807099 created "2016-11-30" @default.
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- W2552807099 date "2016-11-21" @default.
- W2552807099 modified "2023-09-26" @default.
- W2552807099 title "TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells" @default.
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- W2552807099 doi "https://doi.org/10.1038/ni.3630" @default.
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