Molecular basis of DNA recognition in the immune system
dc.contributor.author | Atianand, Maninjay K. | |
dc.contributor.author | Fitzgerald, Katherine A | |
dc.date | 2022-08-11T08:08:24.000 | |
dc.date.accessioned | 2022-08-23T15:53:44Z | |
dc.date.available | 2022-08-23T15:53:44Z | |
dc.date.issued | 2013-03-01 | |
dc.date.submitted | 2013-07-09 | |
dc.identifier.citation | J 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.issn | 0022-1767 (Linking) | |
dc.identifier.doi | 10.4049/jimmunol.1203162 | |
dc.identifier.pmid | 23417527 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/29411 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.url | http://dx.doi.org/10.4049/jimmunol.1203162 | |
dc.subject | Animals | |
dc.subject | Autoimmunity | |
dc.subject | Bacteria | |
dc.subject | Bacterial Infections | |
dc.subject | Cytokines | |
dc.subject | DNA, Bacterial | |
dc.subject | Exodeoxyribonucleases | |
dc.subject | Gene Expression Regulation | |
dc.subject | Host-Pathogen Interactions | |
dc.subject | Humans | |
dc.subject | Immune System | |
dc.subject | *Immunity, Innate | |
dc.subject | Inflammasomes | |
dc.subject | Inflammation | |
dc.subject | Signal Transduction | |
dc.subject | Immunity | |
dc.subject | Immunology and Infectious Disease | |
dc.title | Molecular basis of DNA recognition in the immune system | |
dc.type | Journal Article | |
dc.source.journaltitle | Journal of immunology (Baltimore, Md. : 1950) | |
dc.source.volume | 190 | |
dc.source.issue | 5 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/faculty_pubs/164 | |
dc.identifier.contextkey | 4297374 | |
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.submissionpath | faculty_pubs/164 | |
dc.contributor.department | Department of Medicine, Division of Infectious Diseases and Immunology | |
dc.source.pages | 1911-8 |