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首页> 外文期刊>Cellular immunology >Glucocorticoid receptor mediated suppression of natural killer cell activity: Identification of associated deacetylase and corepressor molecules
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Glucocorticoid receptor mediated suppression of natural killer cell activity: Identification of associated deacetylase and corepressor molecules

机译：糖皮质激素受体介导的自然杀伤细胞活性的抑制：相关脱乙酰酶和共抑制分子的鉴定

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摘要

Physical and psychological stressors reduce natural killer cell function. This reduction in cellular function results from stress-induced release of glucocorticoids. Glucocorticoids act upon natural killer cells to deacetylate and transrepress immune response genes through epigenetic processes. However, other than the glucocorticoid receptor, the proteins that participate in this process are not well described in natural killer cells. The purpose of this study was to identify the proteins associated with the glucocorticoid receptor that are likely epigenetic participants in this process. Treatment of natural killer cells with the synthetic glucocorticoid, dexamethasone, produced a significant time dependent reduction in natural killer cell activity as early as 8. h post treatment. This reduction in natural killer cell activity was preceded by nuclear localization of the glucocorticoid receptor with histone deacetylase 1 and the corepressor, SMRT. Other class I histone deacetylases were not associated with the glucocorticoid receptor nor was the corepressor NCoR. These results demonstrate histone deacetylase 1 and SMRT to associate with the ligand activated glucocorticoid receptor within the nuclei of natural killer cells and to be the likely participants in the histone deacetylation and transrepression that accompanies glucocorticoid mediated reductions in natural killer cell function.
机译：生理和心理压力会降低自然杀伤细胞的功能。细胞功能的这种降低是由于应激诱导释放糖皮质激素引起的。糖皮质激素通过表观遗传过程作用于自然杀伤细胞以脱乙酰化并反抑制免疫反应基因。但是，除了糖皮质激素受体外，在自然杀伤细胞中并未很好地描述参与该过程的蛋白质。本研究的目的是鉴定与糖皮质激素受体相关的蛋白，这些蛋白可能是该过程的表观遗传参与者。用合成的糖皮质激素地塞米松治疗自然杀伤细胞最早可在治疗后8 h产生明显的时间依赖性的自然杀伤细胞活性降低。在自然杀伤细胞活性降低之前，是糖皮质激素受体通过组蛋白脱乙酰基酶1和共抑制因子SMRT的核定位。其他的I类组蛋白脱乙酰基酶与糖皮质激素受体无关，也与NCoR无关。这些结果表明，组蛋白脱乙酰基酶1和SMRT与天然杀伤细胞核内的配体激活的糖皮质激素受体缔合，并且可能是糖皮质激素介导的天然杀伤细胞功能降低中组蛋白脱乙酰化和反式抑制的参与者。

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