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    J Immunol. 2009 Aug 15;183(4):2267-76. Epub 2009 Jul 22.

    Identification of DNA methyltransferase 3a as a T cell receptor-induced regulator of Th1 and Th2 differentiation.

    Gamper CJ, Agoston AT, Nelson WG, Powell JD.

    Department of Oncology, Johns Hopkins University, School of Medicine, Baltimore, MD 21231, USA.

    Ag-specific T cell cytokine expression is dictated by the context in which TCR engagement occurs. Recently it has become clear that epigenetic changes play a role in this process. DNA methyltransferase 3a (DNMT3a) is a de novo methyltransferase important to the epigenetic control of cell fate. We have determined that DNMT3a expression is increased following TCR engagement and that costimulation mitigates DNMT3a protein expression. T cells lacking DNMT3a simultaneously express IFN-gamma and IL-4 after expansion under nonbiasing conditions. While global methylation of DNA from wild-type and knockout T cells is similar, DNMT3a-null T cells demonstrate selective hypomethylation of both the Il4 and Ifng loci after activation. Such hypomethylated knockout Th2 cells retain a greater capacity to express IFN-gamma protein when they are subsequently exposed to Th1-biasing conditions. Based on these findings we propose that DNMT3a is a key participant in regulating T cell polarization at the molecular level by promoting stable selection of a context-specific cell fate through methylation of selective targets in T cells.

    PMID: 19625655 [PubMed - indexed for MEDLINE]

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