Abstract
RIG-I–like receptors (RLRs) are known as viral RNA sensors that trigger the antiviral interferon (IFN) response by the recognition of the nonself signatures in viral RNAs, including 5’ triphosphate structure and double-strand. Self-RNAs generally escape their recognition by several modifications such as 5’ cap; however, it has recently been shown that endogenous RNAs without an adenosine deaminase ADAR1-dependent modification aberrantly activate RLR signalling and lead to severe IFN signature, resulting in autoimmune disorders. Also gain-of-function mutations of RLRs have been found in patients with autoimmune diseases. We herein provide a recent overview of the RLR-mediated antiviral IFN response and autoimmunity and discuss how atypical activation of RLRs triggers autoimmune diseases.
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Kato, H., Fujita, T. (2016). Aberrant Activation of RIG-I–Like Receptors and Autoimmune Diseases. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_39
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