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The association between the mannose-binding lectin codon 54 polymorphism and systemic lupus erythematosus: a meta-analysis update

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dc.contributor.authorLee, Young Ho-
dc.contributor.authorLee, Hye-Soon-
dc.contributor.authorChoi, Sung Jae-
dc.contributor.authorJi, Jong Dae-
dc.contributor.authorSong, Gwan Gyu-
dc.date.accessioned2022-07-16T15:46:07Z-
dc.date.available2022-07-16T15:46:07Z-
dc.date.created2021-05-11-
dc.date.issued2012-05-
dc.identifier.issn0301-4851-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/165744-
dc.description.abstractThe aim of this study was to determine whether the functional mannose-binding lectin (MBL2) exon 1 codon 54 polymorphism (rs1800450) confers susceptibility to systemic lupus erythematosus (SLE) in ethnically different populations. A meta-analysis was conducted on the MBL2 codon 54 polymorphism across 21 comparative studies. Meta-analysis showed an association between the MBL2 codon 54 B allele and SLE in all study subjects [odds ratio (OR) = 1.298, 95% confidence interval (CI) = 1.154-1.459, P = 1.4 x 10(-5)]. Analysis after stratification by ethnicity indicated that the MBL2 codon 54 B allele is significantly associated with SLE in Europeans, Asian, and Africans (OR = 1.246, 95% CI = 1.062-1.462, P = 0.007; OR = 1.268, 95% CI = 1.049-1.532, P = 0.014; OR = 1.939, 95% CI = 1.269-2.962, P = 0.002, respectively). However, African Americans had a much lower prevalence of the T allele (5.8%) than any other populations studied, whereas Asians had the highest prevalence (16.2%). This meta-analysis confirms that the MBL2 codon 54 polymorphism is associated with SLE susceptibility in different ethnic groups, and that its prevalence is ethnicity dependent.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER-
dc.titleThe association between the mannose-binding lectin codon 54 polymorphism and systemic lupus erythematosus: a meta-analysis update-
dc.typeArticle-
dc.contributor.affiliatedAuthorLee, Hye-Soon-
dc.identifier.doi10.1007/s11033-011-1361-6-
dc.identifier.scopusid2-s2.0-84863762526-
dc.identifier.wosid000302147800059-
dc.identifier.bibliographicCitationMOLECULAR BIOLOGY REPORTS, v.39, no.5, pp.5569 - 5574-
dc.relation.isPartOfMOLECULAR BIOLOGY REPORTS-
dc.citation.titleMOLECULAR BIOLOGY REPORTS-
dc.citation.volume39-
dc.citation.number5-
dc.citation.startPage5569-
dc.citation.endPage5574-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.subject.keywordPlusPROTEIN GENE POLYMORPHISM-
dc.subject.keywordPlusRHEUMATOID-ARTHRITIS-
dc.subject.keywordPlusINNATE IMMUNITY-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordPlusDEFICIENCY-
dc.subject.keywordPlusFREQUENCY-
dc.subject.keywordPlusJAPANESE-
dc.subject.keywordPlusTRIALS-
dc.subject.keywordPlusBIAS-
dc.subject.keywordPlusSLE-
dc.subject.keywordAuthorMannose-binding lectin-
dc.subject.keywordAuthorPolymorphism-
dc.subject.keywordAuthorSystemic lupus erythematosus-
dc.subject.keywordAuthorMeta-analysis-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs11033-011-1361-6-
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