Dendritic cell toll-like receptors (TLRs) and the high-affinity immunoglobulin E (IgE) receptor (FcεRI) may biologically interact with regard to atopic dermatitis (AD) development and, especially, severity. Our aim here was to test if such interaction can be detected on the genetic level. The combined effect of the TLR2 gene (TLR2) rs4696480 and the FcεRI α-chain gene (FCER1A) rs2252226 and rs2251746 polymorphisms on the AD severity as measured by SCORAD was assessed. The FCER1A rs2252226 and TLR2 rs4696480 polymorphisms interacted with regard to SCORAD. Higher SCORAD was observed in patients being the TLR2 rs4696480 major homozygotes and carrying at the same time the FCER1A rs2252226 minor allele, compared to those characterized by (any other of) the remaining combined rs2252226 and rs4696480 genotypes. The observation of the epistatic effect of TLR2 and FCER1A genetic variants on SCORAD is in line with the involvement of the interaction TLRs-FcεRI in the pathophysiology of AD.

树突细胞 Toll 样受体 (TLR) 和高亲和力免疫球蛋白 E (IgE) 受体 (FcεRI) 可能与特应性皮炎 (AD) 的发展，尤其是严重程度方面发生生物学相互作用。我们在这里的目的是测试是否可以在基因水平上检测到这种相互作用。所述TLR2基因（的组合效果TLR2）rs4696480和的FcεRIα链基因（FCER1A如由SCORAD测量的AD严重性）rs2252226和rs2251746多态性进行了评估。该FCER1A rs2252226和TLR2 rs4696480多态性与互动方面SCORAD。高SCORAD在患者作为观察TLR2 rs4696480重大纯合子，并在同一时间内携带FCER1Ars2252226 次要等位基因，与那些以（任何其他）剩余组合 rs2252226 和 rs4696480 基因型为特征的基因型相比。观察到TLR2和FCER1A遗传变异对 SCORAD的上位效应与 TLRs-FcεRI 相互作用参与 AD 的病理生理学是一致的。