银屑病发病机制研究进展

Research Progress Etiology and Pathogenesis of Psoriasis

银屑病是一种以表皮增厚、免疫反应和血管增生为特点的疾病。其发病与固有免疫系统和获得性免疫系统相关。其免疫反应发生的中心环节涉及NF-κB,IFN-γ和IL-23信号通路及抗原呈递等多个方面。目前临床上已有如TNF-α、IL-23、IL-17生物靶向治疗取得了很好的疗效,强调了这些炎症介质在临床中的重要性。近几年有研究发现IL-1β/NF-κB通道的激活、IL-23参与胰岛细胞的免疫反应,均可以导致胰岛素抵抗,说明胰岛素抵抗作用可能与了银屑病发病有关。文章就近几年银屑病的发病机制及银屑病相关并发症的研究进展综述如下。

Psoriasis is eharaeterized by the parallel appearanee of epidermal hyperproliferation, inflammation and angioqeo- genesis. It is driven by an intimate interplay between the innate and the adaptive immunesystems. The eentral axes of psoriatic in- flammation enmprises the tmelear factor -kB,inlerferon -g and interleukin （IL） -23 signaling pathways as well as antigen pres- enlation. Biologie therapies targeting tumor neerosis factor- α,lL- 23 or IL- 17 are highly effeetive, underlining the clinical im- portance of these inflammatory mediators. In recent years, Ihere are some sludies have found that the chaunel of IL- 1β/NF - κB aetived and IL - 23 in islet cells of the immune respmse, they can lead to insulin resistance, h suggests thai insulin resistance may be involved in the pathogenesis of psoriasis. In this paper,the etiology and pathogenesis of psoriasis in recent years and the researeh progress of complications associated with psoriasis were reviewed as fi）llows.