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Anti-viral CD8+T cell responses are impaired by endogenous n-3 polyunsaturated fatty acids

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dc.contributor.authorSeo, Young-Jin-
dc.contributor.authorKim, Seyoung-
dc.contributor.authorCho, Yong-Bin-
dc.contributor.authorKang, Kyung-Won-
dc.contributor.authorLee, Sang-Myeong-
dc.date.accessioned2022-01-24T03:43:04Z-
dc.date.available2022-01-24T03:43:04Z-
dc.date.issued2019-05-
dc.identifier.issn0022-1767-
dc.identifier.issn1550-6606-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/54187-
dc.description.abstractOmega-3 (n-3) polyunsaturated fatty acids (PUFAs) have been known to exert anti-inflammatory effects on various inflammatory diseases. However, its role in CD8+ T cell responses against an acute viral infection has not been well elucidated yet. To determine the role of n-3 PUFAs in anti-viral CD8+ T cell responses, we used FAT-1 transgenic mice that are able to convert n-6 PUFAs to n-3 PUFAs. The FAT-1 mice or mice orally administrated with n-3 PFUAs exhibited a significant reduction of anti-viral CD8+ T cell responses against an acute strain of lymphocytic choriomeningitis virus (LCMV). When LCMV-specific P14 CD8+ T cells carrying fat-1 gene (P14/FAT-1) were adoptively transferred into mice that were subsequently infected with LCMV, expansion of the cells was substantially suppressed. Similarly, when P14/FAT-1 cells were stimulated with LCMV gp33 peptide in vitro, their expansion was significantly reduced as compared to P14 cells. Collectively, our results indicate that n-3 PUFAs attenuate anti-viral CD8+ T cell responses against acute viral infection.-
dc.language영어-
dc.language.isoENG-
dc.publisherAMER ASSOC IMMUNOLOGISTS-
dc.titleAnti-viral CD8+T cell responses are impaired by endogenous n-3 polyunsaturated fatty acids-
dc.typeArticle-
dc.identifier.doi10.4049/jimmunol.202.Supp.56.22-
dc.identifier.bibliographicCitationJOURNAL OF IMMUNOLOGY, v.202, no.sup.1-
dc.description.isOpenAccessN-
dc.identifier.wosid000524982500091-
dc.citation.numbersup.1-
dc.citation.titleJOURNAL OF IMMUNOLOGY-
dc.citation.volume202-
dc.type.docTypeMeeting Abstract-
dc.publisher.location미국-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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