干扰素
表观遗传学
生物
IRF5公司
免疫学
先天免疫系统
自身免疫
免疫系统
干扰素调节因子
重编程
遗传学
基因
基因表达
DNA甲基化
作者
Franck J. Barrat,Mary K. Crow,Lionel B. Ivashkiv
出处
期刊:Nature Immunology
[Springer Nature]
日期:2019-11-19
卷期号:20 (12): 1574-1583
被引量:318
标识
DOI:10.1038/s41590-019-0466-2
摘要
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.
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