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Detrimental Type I Interferon Signaling Dominates Protective AIM2 Inflammasome Responses during Francisella novicida Infection
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Zhu, Qifan | - |
dc.contributor.author | Man, Si Ming | - |
dc.contributor.author | Karki, Rajendra | - |
dc.contributor.author | Malireddi, R. K. Subbarao | - |
dc.contributor.author | Kanneganti, Thirumala-Devi | - |
dc.date.accessioned | 2024-05-16T01:58:14Z | - |
dc.date.available | 2024-05-16T01:58:14Z | - |
dc.date.created | 2023-05-08 | - |
dc.date.created | 2023-05-08 | - |
dc.date.issued | 2018-03 | - |
dc.identifier.citation | Cell Reports, Vol.22 No.12, pp.3168-3174 | - |
dc.identifier.issn | 2211-1247 | - |
dc.identifier.uri | https://hdl.handle.net/10371/203035 | - |
dc.description.abstract | Interferons (IFNs) and inflammasomes are essential mediators of anti-microbial immunity. Type I IFN signaling drives activation of the AIM2 inflammasome in macrophages; however, the relative contribution of IFNs and inflammasome responses in host defense is less understood. We report intact AIM2 inflammasome responses in mice lacking type I IFN signaling during infection with F. novicida. Lack of type I IFN signaling conferred protection to F. novicida infection in contrast to the increased susceptibility in AIM2-deficient mice. Mice lacking both AIM2 and IFNAR2 were protected against the infection. The detrimental effects of type I IFN signaling were due to its ability to induce activation of apoptotic caspases and cell death. These results demonstrate the contrasting effects of type I IFN signaling and AIM2 during F. novicida infection in vivo and indicate a dominant role for type I IFNs in mediating detrimental responses despite the protective AIM2 inflammasome responses. | - |
dc.language | 영어 | - |
dc.publisher | Cell Press | - |
dc.title | Detrimental Type I Interferon Signaling Dominates Protective AIM2 Inflammasome Responses during Francisella novicida Infection | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.celrep.2018.02.096 | - |
dc.citation.journaltitle | Cell Reports | - |
dc.identifier.wosid | 000427944200009 | - |
dc.identifier.scopusid | 2-s2.0-85044111271 | - |
dc.citation.endpage | 3174 | - |
dc.citation.number | 12 | - |
dc.citation.startpage | 3168 | - |
dc.citation.volume | 22 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Karki, Rajendra | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | LISTERIA-MONOCYTOGENES | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | LYMPHOCYTES | - |
dc.subject.keywordPlus | TULARENSIS | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordAuthor | AIM2 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | caspase-3 | - |
dc.subject.keywordAuthor | caspase-7 | - |
dc.subject.keywordAuthor | caspase-8 | - |
dc.subject.keywordAuthor | Francisella novicida | - |
dc.subject.keywordAuthor | inflammasomes | - |
dc.subject.keywordAuthor | innate immunity | - |
dc.subject.keywordAuthor | interferon | - |
dc.subject.keywordAuthor | TRAIL | - |
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