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Lee, SangJoon
Viral Immunology Lab.
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DC Field Value Language
dc.citation.number 1 -
dc.citation.startPage 111434 -
dc.citation.title CELL REPORTS -
dc.citation.volume 41 - Wang, Yaqiu - Karki, Rajendra - Mall, Raghvendra - Sharma, Bhesh Raj - Kalathur, Ravi C. - Lee, SangJoon - Kancharana, Balabhaskararao - So, Matthew - Combs, Katie L. - Kanneganti, Thirumala-Devi - 2023-12-21T13:37:47Z - 2023-12-21T13:37:47Z - 2022-10-11 - 2022-10 -
dc.description.abstract Type I interferons (IFNs) are essential innate immune proteins that maintain tissue homeostasis through tonic expression and can be upregulated to drive antiviral resistance and inflammation upon stimulation. However, the mechanisms that inhibit aberrant IFN upregulation in homeostasis and the impacts of tonic IFN production on health and disease remain enigmatic. Here, we report that caspase-8 negatively regulates type I IFN production by inhibiting the RIPK1-TBK1 axis during homeostasis across multiple cell types and tissues. When caspase-8 is deleted or inhibited, RIPK1 interacts with TBK1 to drive elevated IFN production, leading to heightened resistance to norovirus infection in macrophages but also early onset lymphadenopathy in mice. Combined deletion of caspase-8 and RIPK1 reduces the type I IFN signaling and lymphadenopathy, highlighting the critical role of RIPK1 in this process. Overall, our study identifies a mechanism to constrain tonic type I IFN during homeostasis which could be targeted for infectious and inflammatory diseases. -
dc.identifier.bibliographicCitation CELL REPORTS, v.41, no.1, pp.111434 -
dc.identifier.doi 10.1016/j.celrep.2022.111434 -
dc.identifier.issn 2211-1247 -
dc.identifier.scopusid 2-s2.0-85139208583 -
dc.identifier.uri -
dc.identifier.wosid 000869543500006 -
dc.language 영어 -
dc.publisher Cell Press -
dc.title Molecular mechanism of RIPK1 and caspase-8 in homeostatic type I interferon production and regulation -
dc.type Article -
dc.description.isOpenAccess TRUE -
dc.relation.journalWebOfScienceCategory Cell Biology -
dc.relation.journalResearchArea Cell Biology -
dc.type.docType Article -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.subject.keywordPlus INNATE IMMUNITY -
dc.subject.keywordPlus INFLAMMASOME ACTIVATION -
dc.subject.keywordPlus NF-KAPPA-B -
dc.subject.keywordPlus DOMAIN KINASE RIP -


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