IgE FcɛR1β polymorphism and risk of developing chronic spontaneous urticaria: A study in an ethnic Kashmiri population

Abstract

BackgroundThe pathogenesis of chronic spontaneous urticaria involves interplay between the genetic and environmental factors, most of which is still poorly understood. It is well-recognized that 30–40% of chronic spontaneous urticaria is autoimmune in nature. Chronic autoimmune urticaria is caused by anti-FcɛR1β and less frequently, by anti-IgE auto antibodies that lead to mast cell and basophil activation, thereby giving rise to the release of histamine and other proinflammatory mediators. We investigated the association between SNP loci in FcɛR1β and chronic spontaneous urticaria and to see its relation with serum IgE levels in Kashmiri population. MethodsThe autologous serum skin test was used as a screening test for chronic autoimmune urticaria. PCR-RFLP was used to detect the genotype of the SNP loci. Serum IgE levels were assessed by ELISA kit. ResultsNo significant difference was found between the study population and control group in genotype distribution (wild and variant) among FcɛR1β loci (P value=0.06, odds ratio=0.29). The frequency of FcɛR1β (C109T) in autologous serum skin test positive chronic autoimmune urticaria patients with the CT genotype was found to be statistically non-significant when compared with the wild genotype (P=0.35). Carriers of FcɛR1β (T allele) had a more significant risk of developing CAU than those with C allele (P=0.01). In our population serum total IgE levels did not find any statistical significance with regard to ASST positive & ASST negative patients (P=0.26). ConclusionsThere is statistically no significant association between FcɛR1β gene polymorphism and CSU in Kashmiri population; however, there is a probability of developing CSU in patients carrying FcɛR1β T allele. Furthermore, serum total IgE levels had no significant association with the development of CAU.