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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Epigenetic mechanisms of age-dependent KIR2DL4 expression in T cells.
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Epigenetic mechanisms of age-dependent KIR2DL4 expression in T cells.

机译：T细胞中年龄依赖性KIR2DL4表达的表观遗传机制。

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摘要

Killer Ig-like receptor (KIR) expression is mostly restricted to NK cells controlling their activation. With increasing age, KIRs are expressed on T cells and contribute to age-related diseases. We examined epigenetic mechanisms that determine the competency of T cells to transcribe KIR2DL4. Compared with Jurkat cells and CD4(+)CD28(+) T cells from young individuals, DNA methyltransferase (DNMT) inhibition was strikingly more effective in T cells from elderly adults and the CD4(+)CD28(-) T cell line HUT78 to induce KIR2DL4 transcription. In these susceptible cells, the KIR2DL4 promoter was partially demethylated, and dimethylated H3-Lys 4 was increased, and all other histone modifications were characteristic for an inactive promoter. In comparison, NK cells had a fully demethylated KIR2DL4 promoter and the full spectrum of histone modifications indicative of active transcription with H3 and H4 acetylation, di- and trimethylated H3-Lys 4, and reduced, dimethylated H3-Lys 9. These results suggest that anincreased competency of T cells to express KIR2DL4 with aging is conferred by a selective increase in H3-Lys 4 dimethylation and limited DNA demethylation. The partially accessible promoter is sensitive to DNMT inhibition, which is sufficient to induce full transcription without further histone acetylation and methylation.
机译：杀伤性Ig样受体（KIR）的表达主要限于控制其激活的NK细胞。随着年龄的增长，KIRs在T细胞上表达并促进与年龄有关的疾病。我们检查了决定T细胞转录KIR2DL4能力的表观遗传机制。与Jurkat细胞和年轻个体的CD4（+）CD28（+）T细胞相比，DNA甲基转移酶（DNMT）抑制在老年人的T细胞和CD4（+）CD28（-）T细胞系HUT78上显着更有效。诱导KIR2DL4转录。在这些易感细胞中，KIR2DL4启动子被部分去甲基化，而二甲基化的H3-Lys 4增加，所有其他组蛋白修饰是非活性启动子的特征。相比之下，NK细胞具有完全去甲基化的KIR2DL4启动子和完整的组蛋白修饰，表明具有H3和H4乙酰化，二甲基和三甲基化的H3-Lys 4以及还原的二甲基化的H3-Lys 9的活性转录。这些结果表明， H3-Lys 4甲基化的选择性增加和有限的DNA脱甲基化赋予了T细胞随着年龄增长而表达KIR2DL4的能力的增强。部分可进入的启动子对DNMT抑制敏感，该抑制足以诱导完全转录而无需进一步的组蛋白乙酰化和甲基化。

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