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Cited 32 time in webofscience Cited 42 time in scopus
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dc.contributor.authorChang, J-
dc.contributor.authorChoi, SY-
dc.contributor.authorJin, HT-
dc.contributor.authorSung, YC-
dc.contributor.authorBraciale, TJ-
dc.date.accessioned2016-03-31T12:40:55Z-
dc.date.available2016-03-31T12:40:55Z-
dc.date.created2009-02-28-
dc.date.issued2004-01-01-
dc.identifier.issn0022-1767-
dc.identifier.other2004-OAK-0000003891-
dc.identifier.urihttps://oasis.postech.ac.kr/handle/2014.oak/18193-
dc.description.abstractRespiratory syncytial virus (RSV) is a major cause of lower respiratory infection in young children and the elderly. Studies of mice suggest that RSV suppresses the effector activity of CD8 T cells and the development of pulmonary CD8 T cell memory, in which the impaired effector activity could be recovered by in vitro IL-2 treatment. To investigate the effect of in vivo IL-2 expression on RSV immunity, mice were infected with RSV followed by administration of replication-defective adenovirus expressing IL-2. The effector activity of RSV M2-specific CD8 T cells and the development of CD8 T cell memory in the lung was significantly increased by IL-2 expression. Furthermore, the Ab responses against RSV were augmented by IL-2. Interestingly, weight loss and illness caused by RSV challenge were substantially reduced by IL-2 priming, suggesting that the pathogenesis of RSV-related disease could be prevented by IL-2-mediated enhancement of beneficial immune responses. Thus, our results show that IL-2 has potential to be used as a vaccine adjuvant against RSV infection.-
dc.description.statementofresponsibilityX-
dc.languageEnglish-
dc.publisherAMER ASSOC IMMUNOLOGISTS-
dc.relation.isPartOfJOURNAL OF IMMUNOLOGY-
dc.subjectLYMPHOCYTES-
dc.subjectANTIGEN-
dc.subjectINTERLEUKIN-2-
dc.subjectMICE-
dc.subjectEOSINOPHILIA-
dc.subjectIMMUNITY-
dc.subjectDISEASE-
dc.subjectPERSIST-
dc.subjectMAINTENANCE-
dc.subjectACTIVATION-
dc.titleImproved effector activity and memory CD8 T cell development by IL-2 expression during experimental respiratory syncytial virus infection-
dc.typeArticle-
dc.contributor.college생명과학과-
dc.identifier.doi10.4049/jimmunol.172.1.503-
dc.author.googleChang, J-
dc.author.googleChoi, SY-
dc.author.googleJin, HT-
dc.author.googleSung, YC-
dc.author.googleBraciale, TJ-
dc.relation.volume172-
dc.relation.issue1-
dc.relation.startpage503-
dc.relation.lastpage508-
dc.contributor.id10053752-
dc.relation.journalJOURNAL OF IMMUNOLOGY-
dc.relation.indexSCI급, SCOPUS 등재논문-
dc.relation.sciSCI-
dc.collections.nameJournal Papers-
dc.type.rimsART-
dc.identifier.bibliographicCitationJOURNAL OF IMMUNOLOGY, v.172, no.1, pp.503 - 508-
dc.identifier.wosid000187427700062-
dc.date.tcdate2019-01-01-
dc.citation.endPage508-
dc.citation.number1-
dc.citation.startPage503-
dc.citation.titleJOURNAL OF IMMUNOLOGY-
dc.citation.volume172-
dc.contributor.affiliatedAuthorSung, YC-
dc.identifier.scopusid2-s2.0-0347364682-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.wostc26-
dc.type.docTypeArticle-
dc.subject.keywordPlusPERSIST-
dc.subject.keywordPlusMAINTENANCE-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusLYMPHOCYTES-
dc.subject.keywordPlusANTIGEN-
dc.subject.keywordPlusINTERLEUKIN-2-
dc.subject.keywordPlusMICE-
dc.subject.keywordPlusEOSINOPHILIA-
dc.subject.keywordPlusIMMUNITY-
dc.subject.keywordPlusDISEASE-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaImmunology-

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성영철SUNG, YOUNG CHUL
Dept of Life Sciences
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