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Association between the CTLA-4, CD226, FAS polymorphisms and rheumatoid arthritis susceptibility: A meta-analysis

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dc.contributor.authorLee, Young Ho-
dc.contributor.authorBae, Sang-Cheol-
dc.contributor.authorSong, Gwan Gyu-
dc.date.accessioned2021-08-02T18:26:29Z-
dc.date.available2021-08-02T18:26:29Z-
dc.date.issued2015-03-
dc.identifier.issn0198-8859-
dc.identifier.issn1879-1166-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/25629-
dc.description.abstractObjective We explored whether cytotoxic T lymphocyte antigen-4 (CTLA-4) rs5742909, CD226 rs763361, FAS rs1800682, and FASL rs763110 polymorphisms are associated with rheumatoid arthritis (RA). Methods We performed a meta-analysis on the association between the four gene polymorphisms and RA. Results Nineteen studies were included in the meta-analysis. Meta-analysis of all study subjects showed no association between RA and the CTLA-4 rs5742909 T allele (OR = 1.057, 95% CI = 0.782–1.429, p = 0.719). However, the meta-analysis revealed an association between RA and the CD226 rs763361 T allele in all study subjects (OR = 1.294, 95% CI = 1.063–1.576, p = 0.010), and an association was found between the CD226 rs763361 TT genotype and RA in Asians (OR = 1.363, 95% CI = 1.126–1.651, p = 0.001). Meta-analysis showed no association between RA and the FAS rs1800682 G/A polymorphism. However, meta-analysis revealed an association between RA and the FASL rs763110 T allele in all study subjects (OR = 1.366, 95% CI = 1.093–1.707, p = 0.006) and in Asians (OR = 1.402, 95% CI = 1.059–1.855, p = 0.014). Conclusions Our meta-analysis demonstrates that the CD226 rs763361 and FASL rs763110 polymorphisms are associated with RA, especially in Asians.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherElsevier BV-
dc.titleAssociation between the CTLA-4, CD226, FAS polymorphisms and rheumatoid arthritis susceptibility: A meta-analysis-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1016/j.humimm.2015.01.023-
dc.identifier.scopusid2-s2.0-84924043054-
dc.identifier.wosid000350530800003-
dc.identifier.bibliographicCitationHuman Immunology, v.76, no.2-3, pp 83 - 89-
dc.citation.titleHuman Immunology-
dc.citation.volume76-
dc.citation.number2-3-
dc.citation.startPage83-
dc.citation.endPage89-
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.keywordPlusPROMOTER POLYMORPHISM-
dc.subject.keywordPlusAUTOIMMUNE-DISEASES-
dc.subject.keywordPlusGENE POLYMORPHISM-
dc.subject.keywordPlusEXON-1 REGIONS-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusPOPULATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusHAPLOTYPES-
dc.subject.keywordAuthorRheumatoid arthritis-
dc.subject.keywordAuthorCTLA-4-
dc.subject.keywordAuthorCD226-
dc.subject.keywordAuthorFAS-
dc.subject.keywordAuthorPolymorphism-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0198885915000245?via%3Dihub-
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