银屑病发病机制研究进展  

Research progress of pathogenesis of psoriasis

作　　者：马天[1] 姜文成[1] 陈洁[1] 李斌[1] 

机构地区：[1]上海中医药大学附属岳阳中西医结合医院皮肤科,200437

出　　处：《中华临床医师杂志（电子版）》2013年第21期127-128,共2页Chinese Journal of Clinicians(Electronic Edition)

基　　金：国家自然科学基金(81273764);上海市科委中药现代化项目(11DZ1973600);上海市卫生局项目(2011XY004);上海市自然科学基金项目(11ZR1438000);上海市卫生局青年项目(2012QL005A)

摘　　要：银屑病(psoriasis)是多种免疫细胞共同参与的慢性复发性炎症性皮肤病,它具有明显的鳞屑性红斑和不同程度的自觉症状,严重影响患者的生活质量。该病的发病机制探讨多集中在遗传、感染、免疫等方面。目前,越来越多的研究证明了IL-23和CD4阳性辅助性T淋巴细胞17(CD4+T helper 17,Th17)在银屑病病理机制中起到了关键作用。本文就银屑病发病机制的进展作一综述。Psoriasis is one of the most common immune-mediated chronic inflammatory skin disorders associated with the typical erythematous, scaly skin lesions, which can significantly impact quality of life. The pathogenesis of the disease are mainly about genetics, infection and immunity. Recently, more and more research demonstrated that Interleukin-23 （IL-23） and CD4＋ T helper 17 （Thl7） cells were thought to be critical in psoriasis pathogenesis. This review updates the pathogenesis of Psoriasis.

关 键 词：银屑病 白细胞介素23 CD4阳性T淋巴细胞 

分 类 号：R758.63[医药卫生—皮肤病学与性病学]