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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >DNA methylation inhibition increases T cell KIR expression through effects on both promoter methylation and transcription factors.
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DNA methylation inhibition increases T cell KIR expression through effects on both promoter methylation and transcription factors.

机译：DNA甲基化抑制作用通过对启动子甲基化和转录因子的影响来增加T细胞KIR表达。

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摘要

Killer-cell immunoglobulin-like receptor (KIR) genes are a polymorphic family expressed on NK cells, and "senescent" CD28- T cells implicated in cardiovascular disease. KIR promoters are highly homologous, and NK expression is regulated by DNA methylation. T cell KIR regulation is poorly understood. We asked if epigenetic mechanisms and/or transcription factor alterations determine T cell KIR expression. DNA methylation inhibition activated multiple KIR genes in normal T cells. KIR2DL2 and KIR2DL4 were selected for further study. Expression of both was associated with promoter demethylation, and methylation of the promoters in reporter constructs suppressed expression. KIR reporter construct expression also increased in demethylated T cells and required Ets1, Sp1 and AML sites, implying effects on transcription factors. This was confirmed for Sp1. These results indicate that KIR genes are suppressed by DNA methylation in most T cells, and DNA demethylation promotes their expression through effects on both chromatin structure and transcription factors.
机译：杀伤细胞免疫球蛋白样受体（KIR）基因是NK细胞和与心血管疾病有关的“衰老” CD28-T细胞表达的多态家族。 KIR启动子高度同源，NK表达受DNA甲基化调节。 T细胞KIR调节了解甚少。我们询问表观遗传机制和/或转录因子的改变是否决定了T细胞KIR表达。 DNA甲基化抑制激活正常T细胞中的多个KIR基因。选择了KIR2DL2和KIR2DL4进行进一步研究。两者的表达都与启动子去甲基化有关，并且在报告基因构建体中启动子的甲基化抑制了表达。 KIR报告基因构建体的表达在去甲基化T细胞中也增加，并且需要Ets1，Sp1和AML位点，这暗示着对转录因子的影响。 Sp1已得到确认。这些结果表明，在大多数T细胞中，KIR基因被DNA甲基化所抑制，而DNA去甲基化通过对染色质结构和转录因子的影响而促进了它们的表达。

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