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.

中文翻译：

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I 型干扰素和健康和疾病中的内质网应激。

I 型干扰素 (IFN) 由所有有核细胞产生和感知的促炎细胞因子组成，其主要目的是阻止病原体驱动的感染。由于影响范围广泛，I 型干扰素在许多无菌炎症性疾病和免疫病理学中也表现出关键功能，特别是与内质网 (ER) 应激驱动信号通路相关的疾病和免疫病理学。事实上，多年来积累的证据表明，内质网应激的存在可以影响由模式识别受体 (PRR) 激动剂、感染（细菌、病毒或寄生虫）或自身免疫等扰动引起的 I 型干扰素的产生或感知。在本文中，我们讨论了各种疾病背景下 I 型干扰素和 ER 应激之间的联系。我们描述了在微生物感染、自身免疫、糖尿病、癌症和其他与内质网应激相关的情况下，内质网应激如何调节 I 型干扰素的产生或感应，或者 I 型干扰素如何诱导内质网应激。