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Contribution of PTPN22, CD28, CTLA-4 and ZAP-70 variants to the risk of type 1 diabetes in Tunisians
Authors:Ferjeni Zouidi  Mouna Stayoussef  Dorra Bouzid  Hajer Fourati  Olfa Abida  M Ben Ayed  Thouraya Kammoun  Monjia Hachicha  Carlos Penha-Gonçalves  Hatem Masmoudi
Institution:1. Immunology Department, Habib Bourguiba Hospital, Tunisia;2. University of Sfax, Tunisia;3. Pediatric Department, Hedi Chaker Hospital, Tunisia;4. Instituto Gulbenkian de Ciência, Oeiras, Portugal
Abstract: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.
Keywords:T1D  Type 1 diabetes  HWE  Hardy&ndash  Weinberg equilibrium  OR  odds ratios  LD  linkage disequilibrium  haplotype
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