Department for Cellular and Molecular Medicine, Cell Death Research & Therapy (CDRT) Unit, KU Leuven, Leuven, Belgium.
Department for Cellular and Molecular Medicine, Cell Death Research & Therapy (CDRT) Unit, KU Leuven, Leuven, Belgium.
Int Rev Cell Mol Biol. 2020;350:63-118. doi: 10.1016/bs.ircmb.2019.10.004. Epub 2019 Nov 19.
Type I interferons (IFNs) comprise of pro-inflammatory cytokines created, as well as sensed, by all nucleated cells with the main objective of blocking pathogens-driven infections. Owing to this broad range of influence, type I IFNs also exhibit critical functions in many sterile inflammatory diseases and immunopathologies, especially those associated with endoplasmic reticulum (ER) stress-driven signaling pathways. Indeed, over the years accumulating evidence has indicated that the presence of ER stress can influence the production, or sensing of, type I IFNs induced by perturbations like pattern recognition receptor (PRR) agonists, infections (bacterial, viral or parasitic) or autoimmunity. In this article we discuss the link between type I IFNs and ER stress in various diseased contexts. We describe how ER stress regulates type I IFNs production or sensing, or how type I IFNs may induce ER stress, in various circumstances like microbial infections, autoimmunity, diabetes, cancer and other ER stress-related contexts.
I 型干扰素（IFNs）是由所有有核细胞产生和感知的促炎细胞因子，其主要目的是阻止病原体驱动的感染。由于这种广泛的影响，I 型 IFNs 也在许多无菌性炎症性疾病和免疫病理学中表现出关键作用，特别是那些与内质网（ER）应激驱动的信号通路相关的疾病。事实上，多年来的积累证据表明，ER 应激的存在可以影响 I 型 IFNs 的产生或感知，这些 I 型 IFNs 是由模式识别受体（PRR）激动剂、感染（细菌、病毒或寄生虫）或自身免疫等扰动诱导的。在本文中，我们讨论了 I 型 IFNs 与各种疾病环境中的 ER 应激之间的联系。我们描述了 ER 应激如何调节 I 型 IFNs 的产生或感知，或者 I 型 IFNs 如何在微生物感染、自身免疫、糖尿病、癌症和其他与 ER 应激相关的情况下诱导 ER 应激。
