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@ARTICLE{Tsagaratou:119264,
      author       = {A. Tsagaratou and E. González-Avalos and S. Rautio and J.
                      P. Scott-Browne and S. Togher and W. A. Pastor and E. V.
                      Rothenberg and L. Chavez$^*$ and H. Lähdesmäki and A. Rao},
      title        = {{TET} proteins regulate the lineage specification and
                      {TCR}-mediated expansion of i{NKT} cells.},
      journal      = {Nature immunology},
      volume       = {18},
      number       = {1},
      issn         = {1529-2916},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2017-00050},
      pages        = {45 - 53},
      year         = {2017},
      abstract     = {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).},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27869820},
      doi          = {10.1038/ni.3630},
      url          = {https://inrepo02.dkfz.de/record/119264},
}