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dc.contributor.authorFerjeni, Zouidi-
dc.contributor.authorBouzid, D.-
dc.contributor.authorFourati, H.-
dc.contributor.authorStayoussef, M.-
dc.contributor.authorAbida, O.-
dc.contributor.authorKammoun, T.-
dc.contributor.authorHachicha, M.-
dc.contributor.authorPenha-Gonçalves, C.-
dc.contributor.authorMasmoudi, H.-
dc.date.accessioned2018-05-24T14:31:24Z-
dc.date.available2018-05-24T14:31:24Z-
dc.date.issued2015-01-
dc.identifier.citationFerjeni, Z., Bouzid, D., Fourati, H., Stayoussef, M., Abida, O., Kammoun, T., Hachicha, M., Penha-Gonçalves, C., Masmoudi, H. (2015) Association Of Tcr/Cd3, Ptpn22, Cd28 And Zap70 Gene Polymorphisms With Type 1 Diabetes Risk In Tunisian Population: Family Based Association Study. Immunol Lett. 163(1): 1-7.pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/883-
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/S0165247814002594?via%3Dihub#sec0065pt_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 caused by an immune-mediated destruction of the insulin-producing β-cells. Several studies support the involvement of T cell activation molecules in the pathogenesis of T1D. In order to underline the role of the genes involved in this activation pathway, we investigated, using the Sequenom MassARRAY platform, 45 single-nucleotide polymorphisms (SNPs) belonging to TCR/CD3, CD28, ZAP70, and PTPN22 genes in 59 T1D Tunisian families. In the current study, we identified an association with rs706 (Z score=2.782; p=0.005) of TCRβ gene. We also demonstrated that rs10918706 in the intron of the CD3z gene was associated with increased risk of T1D (Z score 2.137; p=0.032). In the same region, rs2949655 (Z score=2.101; p=0.035) and rs1214611 (Z score=4.036; p=0.00005) showed a genotype association with the risk of T1D. When haplotypes were constructed, GAA haplotype displayed significant association with T1D (Z score=2.135; p=0.032), while GGA haplotype (Z score=-1.988; p=0.046) was negatively associated with the disease. We also identified an association with rs3181096 (Z score=2.177; p=0.029), rs17695937 (Z score =2.111; p=0.034) and rs2488457 (Z score=2.219; p=0.026), respectively of CD28, ZAP70 and PTPN22 genes. In addition, our results suggest a significant effect on T1D susceptibility for AC (Z score=2.30; p=0.02) and CTGGC (Z score=2.309, p=0.02) haplotypes of ZAP70 and PTPN22 genes, respectively. While, the GTCT (Z score=-2.114, p=0.034) and CTAGG (Z score=-2.121, p=0.033) haplotypes of CD28 and PTPN22 genes, may confer protection against T1D. These findings confirm the role of PTPN22 and CD28 involved in the T cell activation pathway in the development of T1D in Tunisian families. Interestingly, ZAP70 and TCRβ/CD3z seem to contribute to the susceptibility to the disease in our population. However, this finding has to be confirmed in further studies.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.subjectTCR/CD3pt_PT
dc.subjectPTPN22pt_PT
dc.subjectCD28pt_PT
dc.subjectZAP70pt_PT
dc.subjectTunisiapt_PT
dc.titleAssociation of TCR/CD3, PTPN22, CD28 and ZAP70 gene polymorphisms with type 1 diabetes risk in Tunisian population: Family based association studypt_PT
dc.typearticlept_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
degois.publication.firstPage1pt_PT
degois.publication.issue1pt_PT
degois.publication.lastPage7pt_PT
degois.publication.titleImmunology Letterspt_PT
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0165247814002594?via%3Dihubpt_PT
dc.peerreviewedyespt_PT
degois.publication.volume163pt_PT
dc.identifier.doi10.1016/j.imlet.2014.11.005pt_PT
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