The Role of STING Signaling in Central Nervous System Infection and Neuroinflammatory Disease

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dc.contributor.authorFritsch, Laurenen
dc.contributor.authorKelly, Colinen
dc.contributor.authorPickrell, Alicia M.en
dc.date.accessioned2024-01-23T20:12:18Zen
dc.date.available2024-01-23T20:12:18Zen
dc.date.issued2023-01-12en
dc.description.abstractThe cyclic guanosine monophosphate–adenosine monophosphate (GMP-AMP) synthase-Stimulator of Interferon Genes (cGAS-STING) pathway is a critical innate immune mechanism for detecting the presence of double-stranded DNA (dsDNA) and prompting a robust immune response. Canonical cGAS-STING activation occurs when cGAS, a predominantly cytosolic pattern recognition receptor, binds microbial DNA to promote STING activation. Upon STING activation, transcription factors enter the nucleus to cause the production of Type I interferons, inflammatory cytokines whose primary function is to prime the host for viral infection by producing a number of antiviral interferon-stimulated genes. While the pathway was originally described in viral infection, more recent studies have implicated cGAS-STING signaling in a number of different contexts, including autoimmune disease, cancer, injury, and neuroinflammatory disease. This review focuses on how our understanding of the cGAS-STING pathway has evolved over time with an emphasis on the role of STING-mediated neuroinflammation and infection in the nervous system. We discuss recent findings on how STING signaling contributes to the pathology of pain, traumatic brain injury, and stroke, as well as how mitochondrial DNA may promote STING activation in common neurodegenerative diseases. We conclude by commenting on the current knowledge gaps that should be filled before STING can be an effective therapeutic target in neuroinflammatory disease. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology Infectious Diseases > Molecular and Cellular Physiology Immune System Diseases > Molecular and Cellular Physiology.en
dc.description.versionAccepted versionen
dc.format.extent22 page(s)en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1002/wsbm.1597en
dc.identifier.eissn2692-9368en
dc.identifier.issn2692-9368en
dc.identifier.issue3en
dc.identifier.orcidPickrell, Alicia [0000-0002-8470-6056]en
dc.identifier.pmid36632700en
dc.identifier.urihttps://hdl.handle.net/10919/117627en
dc.identifier.volume15en
dc.language.isoenen
dc.publisherWileyen
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/36632700en
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.subjectbrain injuryen
dc.subjectcGASen
dc.subjectinterferonsen
dc.subjectneuroinflammationen
dc.subjectSTINGen
dc.subjectstrokeen
dc.subject.meshHumansen
dc.subject.meshCentral Nervous System Infectionsen
dc.subject.meshNucleotidyltransferasesen
dc.subject.meshInterferon Type Ien
dc.subject.meshDNAen
dc.subject.meshSignal Transductionen
dc.subject.meshNeuroinflammatory Diseasesen
dc.titleThe Role of STING Signaling in Central Nervous System Infection and Neuroinflammatory Diseaseen
dc.title.serialWIRES Mechanism of Diseaseen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherArticleen
dcterms.dateAccepted2022-12-21en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/Scienceen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Science/COS T&R Facultyen
pubs.organisational-group/Virginia Tech/Science/School of Neuroscienceen

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