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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},
}