Volume 9, Issue 34 (4-2019)                   NCMBJ 2019, 9(34): 93-102 | Back to browse issues page

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Department of Molecular Biology and Genetics, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan Iran.
Abstract:   (2148 Views)
Aim and Background: Multiple sclerosis (MS) is an autoimmune inflammatory disease that attacks myelinated axons in the central nervous system (CNS) resulting in destroying the myelin and the axon. According to high prevalence of disease in Iran, it needs to study different aspects of disease including factors influencing the pathogenesis and the other risk factors. Various type of genetic variants including polymorphisms may could highlight the relation between genetic and disease. In this study, we explored the relationship between IL-4 receptor polymorphism rs1801275 and disease risk.
Material and Methods: In this study, IL-4receptor gene polymorphism was analyzed in a case-control study. All patients were selected as relapsing remitting (RR, n=100) and the control group consisted of 100 healthy (c, n= 100). High resolution melting analysis (HRMA) based on real-time PCR was performed to identify gene variation involved in disease. The results were analyzed by SPSS 20 software and also Hardy Weinberg equilibrium was tested for SNP. Also degree of heterozygosity and population analysis PIC was performed.
Results: The results showed samples from control group consisted of 45% wild genotype (AA), 40% heterozygote (AG) and 15% homozygote (GG) for polymorphism rs1801275 while there was in patient group 20% wild genotype (AA), 58% heterozygote (AG) and 22% homozygote (GG).
Conclusion: These results suggest that there was significant difference in allele count between control and patient groups. The allele frequency of IL-4 receptor polymorphism rs1801275was found significantly higher in patients (P-Value = 0.022). IL4R polymorphisms may have a disease-promoting role in this population.
 
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Type of Study: Research Article | Subject: Cellular and molecular
Received: 2019/03/17 | Accepted: 2019/03/17 | Published: 2019/03/17