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Title: TET proteins regulate lineage specification and TCR-mediated expansion of iNKT cells (ATAC-Seq)      
keywords:
Epigenomics
ID:
PRJNA339230
description:
TET proteins oxidize 5-methylcytosine to 5-hydroxymethylcytosine and further oxidation products in DNA. Here we report that simultaneous deletion of Tet2 and Tet3 in mouse double-positive thymocytes resulted in dysregulated development and proliferation of invariant natural killer T (iNKT) cells. Tet2-Tet3-double-deficient (DKO) iNKT cells displayed pronounced skewing towards 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 uncontrolled expansion dependent on the nonclassical MHC protein CD1d, which presents lipid antigens to iNKT cells. Our data indicate that TET proteins regulate iNKT cell fate by ensuring proper development and maturation and suppressing aberrant T cell antigen receptor (TCR)-mediated proliferation. Overall design: In order to address the impact of the loss of Tet2/3 proteins inchromatin accessibility in iNKT cells we compared by ATACseq thymic wild INKT cells and Tet2/3 DKO iNKT cells
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landingpage: http://www.ncbi.nlm.nih.gov/bioproject/PRJNA339230
authentication:
none
authorization:
none
ID:
pmid:27869820
name:
Mus musculus
ncbiID:
ncbitax:10090
abbreviation:
NCBI
homePage: http://www.ncbi.nlm.nih.gov
ID:
SCR:006472
name:
National Center for Biotechnology Information
homePage: http://www.ncbi.nlm.nih.gov/bioproject
ID:
SCR:004801
name:
NCBI BioProject