特应性皮炎的免疫机制及Dupilumab治疗研究进展

摘要

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.%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 trans-duction,resulting in the occurrence and control chronic inflammation.The update of the immunologic mecha-nism of dupilumab for treating AD is reviewed in this article.