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dc.contributor.authorHosseini, A
dc.contributor.authorShanehbandi, D
dc.contributor.authorEstiar, MA
dc.contributor.authorGholizadeh, S
dc.contributor.authorKhabbazi, A
dc.contributor.authorKhodadadi, H
dc.contributor.authorSakhinia, E
dc.contributor.authorBabaloo, Z
dc.date.accessioned2018-08-26T07:44:37Z
dc.date.available2018-08-26T07:44:37Z
dc.date.issued2015
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/48227
dc.description.abstractBackground: Behcet's Disease (BD) is a rare autoimmune disease that involves the dysfunction of regulatory T cells. FOXP3 is a key transcription factor in the development and function of Treg cells. Recent studies have shown SNPs in the FOXP3 contribute to the susceptibility to some autoimmune disorders. Methods: To clarify the association between the FOXP3 gene and the risk of BD, 50 patients diagnosed with BD and 50 healthy controls from north-western Iran were genotyped by PCR-RFLP (Mun I and Pst I) for two SNPs including rs3761547 (-3499T/C) and rs3761548 (-3279 C/A) in the promoter region of the FOXP3 gene. In addition, a 506 bp nucleotide sequence of FOXP3 promoter was analyzed. Results: The allele -3279 C/A was significantly associated with BD [p = 0.002; odds ratio (OR) = 3.841; 95% confidence interval (Cl) 1.610 - 9.161]; whereas, there was no contribution of the FOXP3 polymorphism -3499T/C to BD [(p = 0.084); (OR = 0.348, 95% CI = 0.101 - 1.195)]. Meanwhile, sequence analysis showed 100% similarity in both controls and BD patient groups. Conclusions: Therefore, the SNP rs3761548 in the FOXP3 gene appears to contribute to the risk of Behcet's disease among the north-western Iranian population.
dc.language.isoEnglish
dc.relation.ispartofCLINICAL LABORATORY
dc.subjectBehcet's disease
dc.subjectsingle nucleotide polymorphism
dc.subjectsequencing
dc.subjectFOXP3
dc.titleA Single Nucleotide Polymorphism in the FOXP3 Gene Associated with Behcet's Disease in an Iranian Population
dc.typeArticle
dc.citation.volume61
dc.citation.issue12
dc.citation.spage1897
dc.citation.epage1903
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.7754/Clin.Lab.2015.150433


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