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Association analysis of −416 G>C polymorphism of T‐cell immunoglobulin and mucin domain‐1 gene with asthma in Iran
Author(s) -
Shirzade H.,
Meshkat R.,
GanjalikhaniHakemi M.,
Mosayebian A.,
Ghasemi R.,
Deress F.,
Parchami barjui S.,
Sadri M.,
Salehi R.
Publication year - 2015
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12209
Subject(s) - mucin , gene , antibody , genetics , biology , asthma , immunology , polymorphism (computer science) , genotype , biochemistry
Summary TIM (T‐cell immunoglobulin (Ig) and mucin domain)‐1, one of the members of TIM family, expresses on Th2 cells and promotes the production of Th2 signature cytokines. This can increase a series of responses in these cells which could be one of the causes of asthma or asthma‐related phenotypes. The aim of this study was to investigate whether a TIM ‐1 promoter single nucleotide polymorphism ( SNP ), −416 G>C, is associated with asthma in Iranian population. In this case–control study, existence of the −416 G>C polymorphism was assessed using polymerase chain reaction ( PCR ) and restriction fragment length polymorphism ( RFLP ) in 300 patients with asthma (97 atopic, 203 nonatopic) and 309 healthy volunteers. Additionally, the relationship between these polymorphism genotypes and total serum IgE levels in this Iranian population was evaluated. We discovered a significant association between the −416 G>C polymorphism and atopic asthma susceptibility in the population, but this SNP showed no connection with nonatopic asthma ( P < 0.05). However, our results showed significant relation between this polymorphism and serum IgE level ( P < 0.05). Our results suggest that −416 G>C polymorphism in TIM ‐1 gene could be a predisposing factor for atopic asthma in Iranian population, and CC genotype of this SNP can be associated with increased level of IgE in patients with asthma in the same population.