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Association between the functional MHC2TA-168 A/G polymorphism and susceptibility to rheumatoid arthritis: a meta-analysis

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dc.contributor.authorLee, Young Ho-
dc.contributor.authorBae, Sang-Cheol-
dc.date.accessioned2021-07-30T05:28:31Z-
dc.date.available2021-07-30T05:28:31Z-
dc.date.issued2016-04-
dc.identifier.issn0770-3198-
dc.identifier.issn1434-9949-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/5075-
dc.description.abstractThe aim of this study was to determine whether the functional major histocompatibility complex II transactivator (MHC2TA) -168 A/G polymorphism is associated with susceptibility to rheumatoid arthritis (RA). A meta-analysis was conducted to estimate the association between the MHC2TA-168 A/G polymorphism and RA. A total of 15 comparative studies, which included 14,158 patients and 13,642 controls, were included in the meta-analysis. Based on the meta-analysis, there was no association between RA and the MHC2TA -168 G allele in the study subjects (OR = 1.046, 95 % CI = 0.987-1.108, p = 0.130) or Caucasians (OR = 1.027, 95 % CI = 0.986-1.070, p = 0.193). However, the country-specific meta-analysis revealed an association between the MHC2TA -168 G allele and RA in the Swedish population (OR = 1.131, 95 % CI = 1.023-1.250, p = 0.016). A direct comparison between rheumatoid factor (RF)-positive and RF-negative patients revealed that the frequency of the G allele was significantly lower in RF-positive patients (OR = 0.783, 95 % CI = 0.628-0.975, p = 0.029) than in RF-negative patients. This meta-analysis demonstrated that the MHC2TA -168 A/G polymorphism is not associated with susceptibility to RA in Caucasians.-
dc.format.extent9-
dc.language영어-
dc.language.isoENG-
dc.publisherSpringer Verlag-
dc.titleAssociation between the functional MHC2TA-168 A/G polymorphism and susceptibility to rheumatoid arthritis: a meta-analysis-
dc.typeArticle-
dc.publisher.location영국-
dc.identifier.doi10.1007/s10067-015-3089-5-
dc.identifier.scopusid2-s2.0-84944549812-
dc.identifier.wosid000373155800010-
dc.identifier.bibliographicCitationClinical Rheumatology, v.35, no.4, pp 901 - 909-
dc.citation.titleClinical Rheumatology-
dc.citation.volume35-
dc.citation.number4-
dc.citation.startPage901-
dc.citation.endPage909-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaRheumatology-
dc.relation.journalWebOfScienceCategoryRheumatology-
dc.subject.keywordPlusMULTIPLE-SCLEROSIS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusPOPULATIONS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusRS3087456-
dc.subject.keywordPlusDISEASES-
dc.subject.keywordAuthorMeta-analysis-
dc.subject.keywordAuthorMHC2TA-
dc.subject.keywordAuthorPolymorphism-
dc.subject.keywordAuthorRheumatoid arthritis-
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