Lack of Association of FOXP3 Gene with Risk of Asthma in Children: A Case-Control Study

Abstract

Background: Loss of Treg cell suppressive activity due to FOXP3 gene disruption is the leading hypothesis for the development of allergy disorders. Thus, asthma susceptibility appears to be determined by host genetic variables affecting FOXP3. A number of research have looked at the role of polymorphisms in the FOXP3 gene in relation to allergy susceptibility. Objective: We aimed at studying the association between FOXP3 gene single nucleotide polymorphism (SNP) and bronchial asthma, asthma severity as well as atopy in Egyptian children. Patients and Methods:The study comprised 101 children with asthma and a control group of 101 children without asthma. Subgroup analyses revealed that there were 44 "atopic" a nd 57 "non-atopic" asthmatics in the total asthmatic group. Polymerase chain reaction sequence specific primers (PCR-SSP) were used to investigate the FOXP3 genotypes (rs3761548, rs2232365). Results: There was no significant difference in the genotypes tested between the asthmatic group and the control group. The AC of rs3761548 and the GG (rs2232365) polymorphisms were the most frequent genotype among the studied children. And only C allele of (rs3761548) was more frequent among asthmatic cases compared to control group. Moreover, no statistically significant difference was found among atopic asthmatic children as regards FOXP3 genotypes (rs3761548, rs2232365) and degree of asthma severity. Conclusions: No link between FOXP3 gene polymorphism (rs3761548 and rs2232365) and asthma susceptibility was found in Egyptian children with asthma. The severity of atopic asthma in children was not shown to be correlated with FOXP3 polymorphism in the present study.