Prevalence of TIM-3 gene polymorphisms in patients with asthma and its correlation with serum levels of immunoglobulin-E of these patients in Isfahan, Iran

Abstract

Background: Asthma is a chronic inflammatory disease of airways and is a multifactorial disease in which, several genes have been identified affecting occurrence and severity of the disease. T-cell immunoglobulin mucin (TIM) gene family that is expressed on T cells and its locus is located on chromosome 5 is one of these genes. A member of the TIM family, TIM-3, is selectively expressed on the surface of differentiated T helper-1 (Th1) cells. Interactions between TIM3 and galectin-9 (TIM3 ligand) regulate Th1 responses and play an important role in the development of allergic disease. Polymorphisms, that affect the structure and function of molecules, may increase the susceptibility to allergic diseases and asthma. In the present study, we assessed the association of the genotype and allele frequencies of the 4259G>T polymorphisms with asthma and the relationships among this polymorphism to IgE levels in patients with asthma. Methods: In this case-control study, we had 209 patients with asthma in case group and 200 healthy people in control group. The variant of genotypes was determined using polymerase chain reaction– restriction fragment length polymorphism (PCR-RFLP) method. The association of this polymorphism and serum immunoglobulin E was analyzed via enzyme-linked immunosorbent assay (ELISA) method. To assess the frequency of genotypes and its relationship with serum immunoglobulin E and asthma, chi-square test was used and P < 0.05 was considered significant. Findings: The genotype and allele frequency of 4259G>T polymorphism were significantly different between the patient and controls. Significant association was observed between this polymorphism and the risk of asthma. Conclusion: The results showed that the 4259G>T polymorphism of TIM3 gene may be associated with the susceptibility of asthma and this polymorphism may affect the performance of TIM3 binding to the ligand molecule (Galectine 9). © 2015, Isfahan University of Medical Sciences(IUMS). All Rights Reserved.