Association between single nucleotide polymorphisms of interleukin-35 genes and atopic dermatitis.

INTRODUCTION

The pathogenesis of atopic dermatitis (AD) involves complex interactions between environmental factors, the skin microbiome, epidermal barrier defects, and altered immune responses that develop on a not fully understood specific genetic background.

AIM

We aimed to evaluate the contribution of single nucleotide polymorphisms (SNPs) in the IL-35 genes ( and ) towards AD susceptibility and clinical characteristics of AD in the Polish population. Two SNPs (rs568408, rs582054) in and one SNP (rs428253) in were selected.

MATERIAL AND METHODS

Blood samples were collected from 202 AD patients and 178 healthy individuals. SNPs in IL-35 genes were analysed by the polymerase chain reaction with sequence-specific primers (SSP-PCR) method.

RESULTS

For rs568408, the AA genotype was significantly linked to increased odds of AD (OR = 34.61; 95% CI: 2.06-579.97, = 0.0137) and marginally associated with normal total serum IgE levels (OR = 2.82; 95% CI: 0.97-8.16; = 0.05), while the GA genotype showed significantly reduced odds of AD (OR = 0.53; 95% CI: 0.34-0.81; = 0.0035). In the context of rs582054, TT genotype carriers had increased odds of AD (OR = 2.05; 95% CI: 1.08-3.85; = 0.03). Patients with the GG genotype of rs428253 had decreased odds of high total serum IgE levels (OR = 0.42; 95% CI: 0.20-0.86; = 0.02) and milder pruritus severity compared to CC genotype carriers (4.12 vs. 7.50; = 0.02).

CONCLUSIONS

IL-35 genetic variations appear to play a role in AD pathogenesis.