| pubmed-article:19625655 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C1743053 | lld:lifeskim |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C1423842 | lld:lifeskim |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
| pubmed-article:19625655 | lifeskim:mentions | umls-concept:C1511938 | lld:lifeskim |
| pubmed-article:19625655 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19625655 | pubmed:dateCreated | 2009-8-7 | lld:pubmed |
| pubmed-article:19625655 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:19625655 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19625655 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19625655 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:19625655 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19625655 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19625655 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:19625655 | pubmed:author | pubmed-author:NelsonWilliam... | lld:pubmed |
| pubmed-article:19625655 | pubmed:author | pubmed-author:PowellJonatha... | lld:pubmed |
| pubmed-article:19625655 | pubmed:author | pubmed-author:AgostonAgosto... | lld:pubmed |
| pubmed-article:19625655 | pubmed:author | pubmed-author:GamperChristo... | lld:pubmed |
| pubmed-article:19625655 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19625655 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:19625655 | pubmed:volume | 183 | lld:pubmed |
| pubmed-article:19625655 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19625655 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19625655 | pubmed:pagination | 2267-76 | lld:pubmed |
| pubmed-article:19625655 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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| pubmed-article:19625655 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19625655 | pubmed:articleTitle | Identification of DNA methyltransferase 3a as a T cell receptor-induced regulator of Th1 and Th2 differentiation. | lld:pubmed |
| pubmed-article:19625655 | pubmed:affiliation | Department of Oncology, Johns Hopkins University, School of Medicine, Baltimore, MD 21231, USA. | lld:pubmed |
| pubmed-article:19625655 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19625655 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:19625655 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19625655 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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