Please use this identifier to cite or link to this item: http://hdl.handle.net/10400.7/886
Title: Contribution of PTPN22, CD28, CTLA-4 and ZAP-70 variants to the risk of type 1 diabetes in Tunisians
Author: Zouidi, Ferjeni
Stayoussef, Mouna
Bouzid, Dorra
Fourati, Hajer
Abida, Olfa
Ayed, M. Ben
Kammoun, Thouraya
Hachicha, Monjia
Penha-Gonçalves, Carlos
Masmoudi, Hatem
Keywords: type 1 diabetes
ZAP-70
CD28
PTPN22
CTLA-4 genes
Tunisia
Issue Date: 1-Jan-2014
Publisher: Elsevier
Citation: 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.
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. 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.
Description: 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
This deposit is composed by the main article, and it hasn't any supplementary materials associated.
This publication hasn't any creative commons license associated.
Peer review: yes
URI: http://hdl.handle.net/10400.7/886
DOI: 10.1016/j.gene.2013.09.112
Publisher Version: https://www.sciencedirect.com/science/article/pii/S0378111913013462?via%3Dihub
Appears in Collections:DG - Artigos em revistas científicas

Files in This Item:
File Description SizeFormat 
Masmoudi,H._Gene_(2014).pdfmain article630,55 kBAdobe PDFView/Open    Request a copy


FacebookTwitterDeliciousLinkedInDiggGoogle BookmarksMySpace
Formato BibTex MendeleyEndnote Degois 

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.