Association between polymorphisms of IL-33 and IL-37 and atopic dermatitis

Abstract

Atopic dermatitis (AD) is a chronic recurrent inflammatory disease accompanied by severe itching. One of the leading mechanisms underlying the development of AD is an imbalance of the Th1/Th2 cells immune response, which leads to an increased production of inflammatory mediators, including IL-1 family. The IL-1 family includes the recently discovered IL-33 and IL-37 and its role in the pathogenesis of AD has been actively studied. IL-33 functions as an alarmin that can induce IL-31 production, thereby leading to skin barrier impairment, pruritus and scratching. Having both immunomodulatory and immunosuppressive properties, IL-37 suppresses leukocyte infiltration of the affected skin and reduces the activity of proinflammatory cytokines. The aim of the research was to find an association between polymorphisms in the genes encoding IL-33, IL-37 and risk of AD. A total of 98 patients with moderate and severe AD were included in the study. The control group included 72 healthy volunteers. Polymorphic markers were determined in peripheral blood. After total RNA extraction, polymorphic markers rs7019575 in the IL-33 gene, rs3811046 and rs3811047 in the IL-37 gene were analyzed using RT-PCR. There was no statistically significant difference in allele frequency and genotype distribution of rs7019575 (IL-33) and rs3811047 (IL-37). The research of the polymorphic marker rs3811046 in the IL-37 gene showed that the risk of AD was almost 2 times lower for the allele G and higher more than 2 times for TT homozygous carriers. The haplotype analysis revealed that the GTAA and TTGG haplotypes of IL-37 were associated with AD, increasing the risk of development by 2 and 10 times, respectively. In conclusion, SNP markers identified in this study can be used to predict the risk of developing AD in individuals with a positive family history of atopic diseases.

Keywords

• atopic dermatitis, tlr, snp, marker, atopic diseases, innate immunity