The interferon (IFN) response, a major vertebrate defense mechanism against viral infections, is initiated by RIG-I-like receptor (RLR)-mediated recognition of viral replicative intermediates in the cytosol. RLR purification methods coupled to RNA sequencing have recently led to the characterization of viral nucleic acid features recognized by RLRs in infected cells. This work revealed that some cellular RNAs can bind to RLRs and stimulate the IFN response. We provide an overview of self and non-self RNAs that activate innate immunity, and discuss the cellular dysregulation that allows recognition of cellular RNAs by RLRs, including RNA mislocalization and downregulation of RNA-shielding proteins. These discussions are relevant because manipulating RLR activation presents opportunities for treating viral infections and autoimmune disorders.

中文翻译：

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宿主和病毒RNA刺激先天免疫。

干扰素（IFN）反应是对抗病毒感染的主要脊椎动物防御机制，是由RIG-1样受体（RLR）介导的对细胞质中病毒复制中间体的识别而引发的。与RNA测序相结合的RLR纯化方法最近已导致表征被感染细胞中RLR识别的病毒核酸特征。这项工作表明，一些细胞RNA可以与RLR结合并刺激IFN反应。我们提供了激活先天性免疫的自我和非自我RNA的概述，并讨论了细胞失调，使RLR识别细胞RNA异常，包括RNA错位和RNA屏蔽蛋白的下调。这些讨论是有意义的，因为操纵RLR激活为治疗病毒感染和自身免疫性疾病提供了机会。