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|Título:||Contribution of PTPN22, CD28, CTLA-4 and ZAP-70 variants to the risk of type 1 diabetes in Tunisians|
Ayed, M. Ben
|Palavras-chave:||type 1 diabetes|
|Citação:||Zouidi, F., Stayoussef, M., Bouzid, D., Fourati, H., Abida, O., Ayed, M.B., Kammoun, T., Hachicha, M., Penha-Gonçalves, C., Masmoudi, H. (2014) Contribution Of Ptpn22, Cd28, Ctla-4 And Zap-70 Variants To The Risk Of Type 1 Diabetes In Tunisians. Gene. 533(1): 420-426.|
|Resumo:||Type 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 order to underline the role of the genes involved in this pathway, we investigated, using the Sequenom MassARRAY platform, polymorphisms of sixteen single-nucleotide polymorphisms (SNPs) belonging to PTPN22, CD28, CTLA-4, and ZAP-70 genes in 76 T1D patients and 162 unrelated healthy controls from Southern Tunisia. We confirmed the association with PTPN22 (rs2476601, Corrected P (Pcorr)=0.002, OR=6.20) and CD28 gene (rs1879877, Pcorr=0.003; OR=4.27 and rs3181096, Pcorr=0.02; OR=1.73). We also identified an association with rs17695937 of ZAP-70 gene (Pcorr=0.02, OR=1.87). Our results suggest a significant effect on T1D susceptibility for A-C-A-G-C and T-C-C-T-A-C haplotypes, of ZAP-70 and CD28 genes, respectively. In addition, (A-G-C) combination of ZAP-70/CD28 gene was significantly increased in T1D patients as compared to controls, suggesting the possible interaction between these genes. These results confirm the involvement of PTPN22 and CD28 genes in the genetic susceptibility to T1D. Interestingly, ZAP-70 seems to contribute to the susceptibility to the disease in our population. However, this finding has to be confirmed in further studies.|
|Descrição:||This 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/S0378111913013462?via%3Dihub#s0060|
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|Versão do Editor:||https://www.sciencedirect.com/science/article/pii/S0378111913013462?via%3Dihub|
|Aparece nas colecções:||DG - Artigos em revistas científicas|
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