DNA methylation and the expanding epigenetics of T cell lineage commitment

被引:111
作者
Wilson, CB [1 ]
Makar, KW
Shnyreva, M
Fitzpatrick, DR
机构
[1] Univ Washington, Dept Immunol & Pediat, Seattle, WA 98195 USA
[2] Dendreon Corp, Seattle, WA 98121 USA
[3] Amgen Inc, Inflammat Res, Seattle, WA 98119 USA
关键词
epigenetic; DNA methylation; histone; chromatin; T cell;
D O I
10.1016/j.smim.2005.01.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
During their development from progenitors, lymphocytes make a series of cell fate decisions. These decisions reflect and require changes in overall programs of gene expression. To maintain cellular identity, programs of gene expression must be iterated through mitosis in a heritable manner by epigenetic processes, which include DNA methylation, methyl-CpG-binding proteins, histone modifications, transcription factors and higher order chromatin structure. Current evidence is consistent with the notion that DNA methylation acts in concert with other epigenetic processes to limit the probability of aberrant gene expression and to stabilize, rather than to initiate, cell fate decisions. In particular, DNA methylation appears to be a non-redundant repressor of CD8 expression in TCR-gamma delta T cells and Th2 cytokine expression in Th1 and CD8 T cells, and is required to enforce clonally restricted Ly49 and KIR gene expression in NK cells. However, most of our knowledge is derived from in vitro studies, and the importance of DNA methylation in memory cell lineage fidelity in vivo remains to be shown convincingly. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:105 / 119
页数:15
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