银屑病同形反应的发病机制研究进展  

Advances in the pathogenesis of psoriasis isomorphism

作　　者：国媛媛 郑庆玲(综述) 曹经江(审校)[1] GUO Yuanyuan;ZHENG Qingling(reviewing);CAO Jingjiang(checking)(Department of Dermatology,Renhe Hospital Affiliated to China Three Gorges University,Yichang 443001,Hubei,China)

机构地区：[1]三峡大学附属仁和医院皮肤科,宜昌443001

出　　处：《医学研究与战创伤救治》2024年第3期327-331,共5页Journal of Medical Research & Combat Trauma Care

基　　金：湖北省教育厅科学研究计划指导性项目(B2015249)。

摘　　要：银屑病作为一种常见的炎症性皮肤疾病,发病机制目前尚不清楚。银屑病的同形反应又称为Koebner现象(KP),是银屑病重要的临床特征之一。目前研究表明银屑病KP的发生可能涉及相关炎症介质(如趋化因子、抗菌肽、类胰蛋白酶)的参与,角质形成细胞(KCs)的增殖与分化异常、机械转导通路作用及血管内皮生成因子的表达增加。文章主要从免疫介导、KCs增殖分化异常、血管增生、机械转导和遗传机制方面对银屑病KP发病机制进行综述。The pathogenesis of psoriasis,which is a common inflammatory skin disease,is still unclear.The psoriasis isomorphism,also known as Koebner phenomenon(KP),is one of the important clinical features of psoriasis.The current study indicates that the pathogenesis of KP in psoriasis may implicate the involvement of relevant inflammatory mediators(e.g.,chemokines,antimicrobial peptides,tryptase),abnormalities in the proliferation and differentiation of Keratinocytes(KCs),the role of mechanical transduction pathways,and the increased expression of vascular endothelial growth factor(VEGF).The paper reviewed the pathogenesis of KP in psoriasis from the perspectives of immune mediation,abnormal proliferation and differentiation of KCs,vascular proliferation,mechanical transduction,and genetic mechanisms.

关 键 词：银屑病 同形反应 发病机制 

分 类 号：R758.63[医药卫生—皮肤病学与性病学]