Interferon target-gene expression and epigenomic signatures in health and disease.,Nature Immunology

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Interferon target-gene expression and epigenomic signatures in health and disease.
Nature Immunology ( IF 27.7 ) Pub Date : 2019-11-19 , DOI: 10.1038/s41590-019-0466-2
Franck J Barrat _{1,

2,

3} , Mary K Crow _{1,

3,

4} , Lionel B Ivashkiv _{1,

3,

4}

Affiliation

Multiple type I interferons and interferon-γ (IFN-γ) are expressed under physiological conditions and are increased by stress and infections, and in autoinflammatory and autoimmune diseases. Interferons activate the Jak-STAT signaling pathway and induce overlapping patterns of expression, called 'interferon signatures', of canonical interferon-stimulated genes (ISGs) encoding molecules important for antiviral responses, antigen presentation, autoimmunity and inflammation. It has now become clear that interferons also induce an 'interferon epigenomic signature' by activating latent enhancers and 'bookmarking' chromatin, thus reprogramming cell responses to environmental cues. The interferon epigenomic signature affects ISGs and other gene sets, including canonical targets of the transcription factor NF-κB that encode inflammatory molecules, and is involved in the priming of immune cells, tolerance and the training of innate immune memory. Here we review the mechanisms through which interferon signatures and interferon epigenomic signatures are generated, as well as the expression and functional consequences of these signatures in homeostasis and autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis and systemic sclerosis.

中文翻译：

干扰素靶基因表达和健康和疾病中的表观基因组特征。

多种 I 型干扰素和干扰素-γ (IFN-γ) 在生理条件下表达，并在压力和感染以及自身炎症和自身免疫疾病中增加。干扰素激活 Jak-STAT 信号通路并诱导经典干扰素刺激基因 (ISG) 的重叠表达模式，称为“干扰素特征”，这些基因编码对抗病毒反应、抗原呈递、自身免疫和炎症很重要的分子。现在已经清楚，干扰素还通过激活潜在增强子和“标记”染色质来诱导“干扰素表观基因组特征”，从而重新编程细胞对环境线索的反应。干扰素表观基因组特征影响 ISG 和其他基因组，包括编码炎症分子的转录因子 NF-κB 的典型靶标，并参与免疫细胞的启动、耐受性和先天免疫记忆的训练。在这里，我们回顾了产生干扰素特征和干扰素表观基因组特征的机制，以及这些特征在体内平衡和自身免疫性疾病（包括系统性红斑狼疮、类风湿性关节炎和系统性硬化症）中的表达和功能后果。

更新日期：2019-11-20

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