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dc.contributor.author Lee, Jinhee -
dc.contributor.author Jang, Soyoung -
dc.contributor.author Choi, Minjee -
dc.contributor.author Kang, Mincheol -
dc.contributor.author Lim, Su-Geun -
dc.contributor.author Kim, SI-Yong -
dc.contributor.author Jang, Soyeon -
dc.contributor.author Ko, Jiwon -
dc.contributor.author Kim, Eungyung -
dc.contributor.author Yi, Junkoo -
dc.contributor.author Choo, Yeonsik -
dc.contributor.author Kim, Myoung Ok -
dc.contributor.author Ryoo, Zae Young -
dc.date.accessioned 2021-10-15T06:00:09Z -
dc.date.available 2021-10-15T06:00:09Z -
dc.date.created 2021-08-19 -
dc.date.issued 2021-08 -
dc.identifier.citation Scientific Reports, v.11, no.1, pp.16348 -
dc.identifier.issn 2045-2322 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/15505 -
dc.description.abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms. © 2021, The Author(s). -
dc.language English -
dc.publisher Nature Research -
dc.title Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice -
dc.type Article -
dc.identifier.doi 10.1038/s41598-021-94855-5 -
dc.identifier.wosid 000684343800082 -
dc.identifier.scopusid 2-s2.0-85112305210 -
dc.type.local Article(Overseas) -
dc.type.rims ART -
dc.description.journalClass 1 -
dc.citation.publicationname Scientific Reports -
dc.contributor.nonIdAuthor Lee, Jinhee -
dc.contributor.nonIdAuthor Jang, Soyoung -
dc.contributor.nonIdAuthor Choi, Minjee -
dc.contributor.nonIdAuthor Kang, Mincheol -
dc.contributor.nonIdAuthor Lim, Su-Geun -
dc.contributor.nonIdAuthor Kim, SI-Yong -
dc.contributor.nonIdAuthor Jang, Soyeon -
dc.contributor.nonIdAuthor Ko, Jiwon -
dc.contributor.nonIdAuthor Kim, Eungyung -
dc.contributor.nonIdAuthor Yi, Junkoo -
dc.contributor.nonIdAuthor Choo, Yeonsik -
dc.contributor.nonIdAuthor Kim, Myoung Ok -
dc.contributor.nonIdAuthor Ryoo, Zae Young -
dc.identifier.citationVolume 11 -
dc.identifier.citationNumber 1 -
dc.identifier.citationStartPage 16348 -
dc.identifier.citationTitle Scientific Reports -
dc.description.isOpenAccess Y -
dc.subject.keywordPlus I INTERFERONAUTOANTIBODIESERYTHEMATOSUSMECHANISMSINDUCTIONPRISTANEDISEASEMODELSCELLS -
dc.contributor.affiliatedAuthor Lee, Jinhee -
dc.contributor.affiliatedAuthor Jang, Soyoung -
dc.contributor.affiliatedAuthor Choi, Minjee -
dc.contributor.affiliatedAuthor Kang, Mincheol -
dc.contributor.affiliatedAuthor Lim, Su-Geun -
dc.contributor.affiliatedAuthor Kim, SI-Yong -
dc.contributor.affiliatedAuthor Jang, Soyeon -
dc.contributor.affiliatedAuthor Ko, Jiwon -
dc.contributor.affiliatedAuthor Kim, Eungyung -
dc.contributor.affiliatedAuthor Yi, Junkoo -
dc.contributor.affiliatedAuthor Choo, Yeonsik -
dc.contributor.affiliatedAuthor Kim, Myoung Ok -
dc.contributor.affiliatedAuthor Ryoo, Zae Young -
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