IgE在湿疹发病中的作用机制

Role of immunoglobulin E in atopic dermatitis

免疫球蛋白E(IgE)在湿疹等许多自身过敏性疾病的发病机制中扮演重要角色。研究发现,IgE主要通过其在肥大细胞、嗜碱性细胞等细胞上的高亲和力受体FcεRⅠ及低亲和力受体FcεRⅡ(CD23)发挥作用,此外还能通过半乳糖凝集素-3信号通路活化肥大细胞和嗜碱性细胞,最终导致自身免疫性疾病的发生。本文对近期相关文献进行综述,对IgE在湿疹等自身免疫相关性疾病中发挥的作用和可能发病机制进行分析,以期为日后药物研发和临床工作提供指导。

Immunoglobulin E(IgE)plays an important role in the pathogenesis of many autoallergic diseases such as eczema.The study found that the IgE play a role mainly through its high affinity receptor FcεRⅠand low affinity receptors epsilon FcεRⅡ(CD23)in mast cells and basophilic cells,In addition,mast cells and basophilic cells can be activated by the galactosin-3 signaling pathway,eventually lead to the occurrence of autoimmune diseases.This paper reviews the recent literature and analyzes the role and possible pathogenesis of Ig E in autoimmune diseases such as eczema,in order to provide guidance for future drug development and clinical work.