特应性皮炎的免疫机制及Dupilumab治疗研究进展

Ⅱ型辅助性T细胞（Th2）在特应性皮炎（AD）皮损中显著增高,并促进IL-4和IL-13的分泌,通过共受体IL-4Rα介导下游信号转导。目前多种新型免疫抑制剂已在治疗AD的临床研究中,其中Dupilumab 是抗 IL-4 受体α亚基（IL-4Rα）的单克隆抗体,能竞争性抑制IL-4、IL-13与IL-4Rα结合并阻断其介导的下游信号转导,从而抑制皮肤慢性炎症的发生发展。 本文综述了特应性皮炎的免疫学发病机制及靶向生物制剂Dupilumab治疗的研究现状。

Immune mechanism and clinical research progress in the treatment of atopic dermatitis with dupilumab

The level of Th2 cells is increased in the lesions of atopic dermatitis (AD) and the Th2 cells can stimulate the secretion of IL-4 and IL-13. IL-4 and IL-13 can mediate the downstream signal transduction through the co-receptor IL-4Rα. A variety of new targeted immunosuppressive agents have been used in the clinical study of AD. Dupilumab is a monoclonal antibody to the anti-IL-4 receptor alpha subunit (IL-4Ralpha), which can inhibit IL-4 and IL-13 to bind to IL-4Ralpha and block its downstream signal transduction, resulting in the occurrence and control chronic inflammation. The update of the immunologic mechanism of dupilumab for treating AD is reviewed in this article.