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功能性 FCER1A 和 TLR2 多态性与特应性皮炎严重程度的相互作用。

Interaction between functional polymorphisms in FCER1A and TLR2 and the severity of atopic dermatitis.

机构信息

Institute of Laboratory Medicine and Pathobiochemistry, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL), Philipps University Marburg, Marburg, Germany; Krakow Center for Medical Research and Technology, John Paul II Hospital, Krakow, Poland.

Krakow Center for Medical Research and Technology, John Paul II Hospital, Krakow, Poland.

出版信息

Hum Immunol. 2020 Dec;81(12):709-713. doi: 10.1016/j.humimm.2020.08.002. Epub 2020 Sep 1.

DOI:10.1016/j.humimm.2020.08.002
PMID:32883546
Abstract

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.

摘要

树突状细胞 Toll 样受体 (TLR) 和高亲和力免疫球蛋白 E (IgE) 受体 (FcεRI) 可能在特应性皮炎 (AD) 的发展,特别是严重程度方面具有生物学相互作用。我们的目的是检验这种相互作用是否可以在遗传水平上被检测到。通过 SCORAD 评估 TLR2 基因 (TLR2) rs4696480 和 FcεRIα 链基因 (FCER1A) rs2252226 和 rs2251746 多态性对 AD 严重程度的联合影响。评估了 FCER1A rs2252226 和 TLR2 rs4696480 多态性之间关于 SCORAD 的相互作用。与具有任何其他 rs2252226 和 rs4696480 基因型的患者相比,TLR2 rs4696480 主要纯合子且同时携带 FCER1A rs2252226 次要等位基因的患者的 SCORAD 更高。TLR2 和 FCER1A 遗传变异对 SCORAD 的上位性效应的观察结果与 TLRs-FcεRI 的相互作用在 AD 病理生理学中的参与一致。

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