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Cited 12 time in webofscience Cited 12 time in scopus
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Interleukin-4, interleukin-4 receptor, and interleukin-18 polymorphisms and rheumatoid arthritis: a meta-analysis

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dc.contributor.authorSong, Gwan Gyu-
dc.contributor.authorBae, Sang-Cheol-
dc.contributor.authorKim, Jae-Hoon-
dc.contributor.authorLee, Young Ho-
dc.date.accessioned2021-08-02T18:55:32Z-
dc.date.available2021-08-02T18:55:32Z-
dc.date.issued2013-07-
dc.identifier.issn0882-0139-
dc.identifier.issn1532-4311-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/26681-
dc.description.abstractObjective: The aim of this study was to determine whether the functional interleukin-4 (IL-4) -590 C/T, IL-4 receptor (IL-4R) 1902 G/A, IL-18 -607 C/A, and -137 G/C polymorphisms polymorphisms confer susceptibility to rheumatoid arthritis (RA). Methods: Meta-analysis was conducted on the associations between these IL-4, IL-4R, and IL-18 polymorphisms and RA. Results: A total of 12 comparative studies were included in this meta-analysis. Meta-analysis of the IL-4 -590 C/T polymorphism showed an association in all study subjects and Europeans (OR for the TT genotype = 2.280, 95% CI = 1.315-3.952, p = 0.003; OR = 2.139, 95% CI = 1.089-4.199, p = 0.027). However, meta-analysis showed no association between RA and the IL-4R 1902 G allele in all study subjects and Europeans. Meta-analysis showed no association between RA and the IL-18 -607 C allele (OR = 1.159, 95% CI = 0.967-1.387, p = 0.110). Meta-analysis of the IL-18 -137 G/C polymorphism revealed no association between RA and the IL-18 -137 G/C polymorphism. Conclusions: This meta-analysis demonstrates that the IL-4 -590 T/C polymorphism is associated with susceptibility to RA in Europeans, but the IL-4R+1902 G/A, IL-18 -607 C/A and -137 G/C polymorphisms are not associated with RA.-
dc.format.extent15-
dc.language영어-
dc.language.isoENG-
dc.publisherMarcel Dekker Inc.-
dc.titleInterleukin-4, interleukin-4 receptor, and interleukin-18 polymorphisms and rheumatoid arthritis: a meta-analysis-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.3109/08820139.2013.804084-
dc.identifier.scopusid2-s2.0-84880895470-
dc.identifier.wosid000322178000001-
dc.identifier.bibliographicCitationImmunological Investigations, v.42, no.6, pp 455 - 469-
dc.citation.titleImmunological Investigations-
dc.citation.volume42-
dc.citation.number6-
dc.citation.startPage455-
dc.citation.endPage469-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.subject.keywordPlusSYSTEMIC-LUPUS-ERYTHEMATOSUS-
dc.subject.keywordPlusSINGLE-NUCLEOTIDE POLYMORPHISMS-
dc.subject.keywordPlusPROMOTER POLYMORPHISM-
dc.subject.keywordPlusGENE POLYMORPHISMS-
dc.subject.keywordPlusIL-6 GENE-
dc.subject.keywordPlusASSOCIATION-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusTRANSCRIPTION-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordAuthorinterleukin-4-
dc.subject.keywordAuthorIL-18-
dc.subject.keywordAuthorpolymorphism-
dc.subject.keywordAuthorrheumatoid arthritis-
dc.subject.keywordAuthormeta-analysis-
dc.identifier.urlhttps://www.tandfonline.com/doi/full/10.3109/08820139.2013.804084-
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