Nucleic Acid Sensing and Innate Immunity: Signaling Pathways Controlling Viral Pathogenesis and Autoimmunity
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Innate immunity refers to the body’s initial response to curb infection upon exposure to invading organisms. While the detection of pathogen-associated molecules is an ancient form of host defense, if dysfunctional, autoimmune disease may result. The innate immune response during pathogenic infection is initiated through the activation of receptors recognizing conserved molecular patterns, such as nucleic acids from a virus’ genome or replicative cycle. Additionally, the host’s own nucleic acids are capable of activating an immune response. Therefore, it follows that the nucleic acid-sensing pathways must be tightly controlled to avoid an autoimmune response from recognition of self, yet still be unimpeded to respond to viral infections. In this review, we will describe the nucleic acid sensing pathways and how they respond to virus infection. Moreover, we will discuss autoimmune diseases that develop when these pathways fail to signal properly and identify knowledge gaps that are prime for interrogation.
KeywordsAutoimmunity Interferon RIG-I MDA5 STING cGAS
Research in the Goodman Lab is funded by NIH Grant R00 AI106963 and funds from Washington State University. L.R.H. Ahlers is supported by NIH Training Grant T32 GM008336.
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Conflict of Interest
Laura Ahlers and Alan Goodman declare that they have no conflict of interest.
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This article does not contain any studies with human or animal subjects performed by any of the authors.
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