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首页> 外文期刊>Nature clinical practice. Rheumatology >Primer: epigenetics of autoimmunity.
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Primer: epigenetics of autoimmunity.

机译：引物：自身免疫的表观遗传学。

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Interactions between environmental and genetic factors are proposed to explain why autoimmunity afflicts certain individuals and not others. Genes and genetic loci predisposing to autoimmunity are being identified, but theories as to how the environment contributes to autoimmunity still rely largely on examples such as drug-induced systemic lupus erythematosus (SLE) and epidemiologic evidence of occupational exposure, without clear mechanistic explanations or identification of specific environmental agents. Eukaryotic gene expression requires not only transcription factor activation but also regional modification of chromatin structure into a transcriptionally permissive configuration through epigenetic mechanisms, including DNA methylation and histone modifications. The realization that epigenetic mechanisms can alter gene expression and, therefore, cellular function has led to new insights into how environmental agents might contribute to the development of diseases in genetically predisposed individuals. The observation that some SLE-inducing drugs, such as procainamide and hydralazine, affect T cell DNA methylation and thereby cellular function, and that identical changes in T cell DNA methylation and cellular function are found in patients with SLE, implicates epigenetic mechanisms in the pathogenesis of human SLE, and perhaps other autoimmune diseases. In this Review we discuss how epigenetic mechanisms affect gene expression, how environmental agents can affect epigenetic mechanisms, and how epigenetic changes in gene expression can contribute to autoimmunity. Similar mechanisms might also contribute to the pathogenesis of other poorly understood human diseases.
机译：提出了环境和遗传因素之间的相互作用来解释为什么自身免疫会影响某些人而不是其他人。易患自身免疫的基因和基因位点已被确定，但有关环境如何促进自身免疫的理论仍主要依靠诸如药物诱发的系统性红斑狼疮（SLE）和职业暴露的流行病学证据等例子，而没有明确的机理解释或鉴定。特定的环保剂。真核基因表达不仅需要转录因子激活，而且还需要通过表观遗传机制将染色质结构的区域修饰成转录允许的构型，包括DNA甲基化和组蛋白修饰。表观遗传机制可以改变基因表达，进而改变细胞功能，这一认识使人们对环境因素如何促进遗传易感人群中疾病的发展有了新的认识。观察发现，某些SLE诱导药物，如普鲁卡因胺和肼苯哒嗪，会影响T细胞DNA甲基化并进而影响细胞功能，并且在SLE患者中发现T细胞DNA甲基化和细胞功能的相同变化，暗示了发病机理中的表观遗传机制。人类SLE以及其他自身免疫性疾病。在本综述中，我们讨论了表观遗传机制如何影响基因表达，环境因素如何影响表观遗传机制以及基因表达的表观遗传变化如何有助于自身免疫。相似的机制也可能导致其他人们了解程度较低的人类疾病的发病机理。

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