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dc.contributor.authorAtianand, Maninjay K.
dc.contributor.authorFitzgerald, Katherine A
dc.date2022-08-11T08:08:24.000
dc.date.accessioned2022-08-23T15:53:44Z
dc.date.available2022-08-23T15:53:44Z
dc.date.issued2013-03-01
dc.date.submitted2013-07-09
dc.identifier.citationJ Immunol. 2013 Mar 1;190(5):1911-8. doi: 10.4049/jimmunol.1203162. <a href="http://dx.doi.org/10.4049/jimmunol.1203162" target="_blank">Link to article on publisher's site</a>
dc.identifier.issn0022-1767 (Linking)
dc.identifier.doi10.4049/jimmunol.1203162
dc.identifier.pmid23417527
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29411
dc.description.abstractRecognition of microbial nucleic acids is one strategy by which mammalian hosts respond to infectious agents. Intracellular DNA that is introduced into cells during infection elicits potent inflammatory responses by triggering the induction of antiviral type I IFNs and the maturation and secretion of inflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-18. In addition, if nucleases, such as DNase II or DNase III (Trex1), fail to clear self-DNA, accumulated DNA gains access to intracellular compartments where it drives inflammatory responses leading to autoimmune disease. In this review, we discuss a rapidly evolving view of how cytosolic DNA-sensing machineries coordinate antimicrobial immunity and, if unchecked, lead to autoimmune disease.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23417527&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.4049/jimmunol.1203162
dc.subjectAnimals
dc.subjectAutoimmunity
dc.subjectBacteria
dc.subjectBacterial Infections
dc.subjectCytokines
dc.subjectDNA, Bacterial
dc.subjectExodeoxyribonucleases
dc.subjectGene Expression Regulation
dc.subjectHost-Pathogen Interactions
dc.subjectHumans
dc.subjectImmune System
dc.subject*Immunity, Innate
dc.subjectInflammasomes
dc.subjectInflammation
dc.subjectSignal Transduction
dc.subjectImmunity
dc.subjectImmunology and Infectious Disease
dc.titleMolecular basis of DNA recognition in the immune system
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume190
dc.source.issue5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/164
dc.identifier.contextkey4297374
html.description.abstract<p>Recognition of microbial nucleic acids is one strategy by which mammalian hosts respond to infectious agents. Intracellular DNA that is introduced into cells during infection elicits potent inflammatory responses by triggering the induction of antiviral type I IFNs and the maturation and secretion of inflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-18. In addition, if nucleases, such as DNase II or DNase III (Trex1), fail to clear self-DNA, accumulated DNA gains access to intracellular compartments where it drives inflammatory responses leading to autoimmune disease. In this review, we discuss a rapidly evolving view of how cytosolic DNA-sensing machineries coordinate antimicrobial immunity and, if unchecked, lead to autoimmune disease.</p>
dc.identifier.submissionpathfaculty_pubs/164
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages1911-8


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