Volume 16, Issue 62 (7-2007)                   JGUMS 2007, 16(62): 1-6 | Back to browse issues page

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Masood M, Salehi E, Sheykh Bahayi N, Rajab A, Vojgani M, Massoud A. Survey the Single Nucleotide Polymorphism of TGFβ at Codon 25 in Type 1 Diabetic Patients. JGUMS 2007; 16 (62) :1-6
URL: http://journal.gums.ac.ir/article-1-374-en.html
1- , massoud ah_2002@yahoo.com
Abstract:   (7162 Views)
Abstract Introduction: Type 1 diabetes is an autoimmune disease which is characterized by T-cell mediated destruction of pancreatic β-cells. A variety of environmental and genetic factors are involved in the development of the disease. Transforming Growth Factor Beta-1 (TGFβ) is a multifunctional cytokine that affected regulation and difference of immune responses and there is abnormal secretion of this auto immune disease. Genetic polymorphisms in the TGFβ gene influenced production and secretion of cytokine and figured as a risk factor in auto immune disease. Objective: In this study, single nucleotide polymorphism of TGFβ at codon 25 is investigated in type 1 diabetic patients and compared with healthy controls. Materials and Methods: This was a case control study which 75 type 1 diabetic patients who had definitely diagnosed at least 2 years before sampling and were under Insulin therapy were selected. Control group were selected from voluntarily blood donors who had referred to IRAN Blood Transfusion Organization. Data were analyzed by SPSS and using chi- square test with 95% confidence interval. Results: The findings showed that there were not statistically significant differences in G C polymorphism at +915 between cases and control groups (p value 0.05). Conclusion Although TGFβ polymorphism at +915 regions affects the production of cytokine regulates immune responses this study showed that single nucleotide polymorphism in this region can not be involved in onset of type 1diabetes and can not be considered as risk factor.
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Review Paper: Research | Subject: Special
Received: 2013/12/29 | Accepted: 2013/12/29 | Published: 2013/12/29

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