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).