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dc.contributor.authorZouidi, Ferjani-
dc.contributor.authorStayoussef, Mouna-
dc.contributor.authorBouzid, Dorra-
dc.contributor.authorFourati, Hajer-
dc.contributor.authorAbida, Olfa-
dc.contributor.authorJoão, Costa-
dc.contributor.authorAyed, Mourad Ben-
dc.contributor.authorFakhfakh, Raouia-
dc.contributor.authorThouraya, Kammoun-
dc.contributor.authorMonjia, Hachicha-
dc.contributor.authorCarlos, Penha-Gonçalves-
dc.contributor.authorMasmoudi, Hatem-
dc.date.accessioned2018-05-25T11:55:29Z-
dc.date.available2018-05-25T11:55:29Z-
dc.date.issued2014-02-25-
dc.identifier.citationZouidi, F., Stayoussef, M., Bouzid, D., Fourati, H., Abida, O., João, C., Ayed, M.B., Fakhfakh, R., Thouraya, K., Monjia, H., Carlos, P., Masmoudi, H. (2014) Association Of Bank1 And Cytokine Gene Polymorphisms With Type 1 Diabetes In Tunisia. Gene. 536(2): 296-301.pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/885-
dc.descriptionThis deposit is composed by a publication in which the IGC's authors have had the role of collaboration (it's a collaboration publication). This type of deposit in ARCA is in restrictedAccess (it can't be in open access to the public), and can only be accessed by two ways: either by requesting a legal copy from the author (the email contact present in this deposit) or by visiting the following link: https://www.sciencedirect.com/science/article/pii/S0378111913016545?via%3Dihub#ac0005pt_PT
dc.descriptionThis deposit is composed by the main article, and it hasn't any supplementary materials associated.pt_PT
dc.descriptionThis publication hasn't any creative commons license associated.pt_PT
dc.description.abstractType 1 diabetes (T1D) is an autoimmune disease (AID) with both genetic and environmental components. We aimed to investigate the genetic association of polymorphisms in genes previously linked with other AIDs, namely BANK1, IL15 and IL2/IL21 region. A total of 76 T1D patients and 162 controls from Southern Tunisia were recruited for a case-control association study investigating the relationship between sixteen SNPs of the BANK1, IL15 and IL2/IL21 gene region and T1D. In the BANK1 gene, G allele and GG genotype of rs3733197 were significantly increased in the group of T1D patients compared to controls. In addition, in the IL15 gene, the minor allele A of rs10519613 polymorphism was significantly higher in patients than in controls. No significant association was found for SNPS in IL2/IL21 gene region. The analysis of the haplotype structure revealed the G-C-A-C-T haplotype of the IL15 gene as associated with a reduction in the risk of developing T1D, while A-T-A-C-T haplotype increased the risk of developing the disease. Furthermore, in the IL2/IL21 region, only one haplotype consisting of eight SNPs was markedly associated with T1D susceptibility. Moreover, G-C combination of the BANK1/IL15 was significantly increased in T1D patients, compared to controls. Our results establish BANK1 and IL15 as new T1D genetic susceptibility factors and replicate the association of the 4q27 region with T1D. Our data agree with the effect previously observed for other autoimmune conditions and delineate a shared underlying mechanism.pt_PT
dc.description.sponsorshipThere are no funders and sponsors indicated explicitly in the document.pt_PT
dc.language.isoengpt_PT
dc.publisherElsevierpt_PT
dc.relationThere are no funders and sponsors indicated explicitly in the document.pt_PT
dc.rightsrestrictedAccesspt_PT
dc.subjectType 1 diabetespt_PT
dc.subjectBANK1pt_PT
dc.subjectCytokine genespt_PT
dc.subjectTunisiapt_PT
dc.titleAssociation of BANK1 and cytokine gene polymorphisms with type 1 diabetes in Tunisiapt_PT
dc.typearticlept_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
degois.publication.firstPage296pt_PT
degois.publication.issue2pt_PT
degois.publication.lastPage301pt_PT
degois.publication.titleGenept_PT
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0378111913016545?via%3Dihubpt_PT
dc.peerreviewedyespt_PT
degois.publication.volume536pt_PT
dc.identifier.doi10.1016/j.gene.2013.12.008pt_PT
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