摘要
咪喹莫特作为治疗人乳头瘤病毒感染的药物，在临床应用中发现可引起银屑病样皮损并能加重银屑病患者病情，而被广泛用于银屑病发病机制及治疗靶点的研究。由咪喹莫特诱发的小鼠银屑病样模型具有操作简单、易于成模的优点。应用咪喹莫特后，小鼠体内有包括Toll样受体信号通路等多条通路被激活，其中部分为协同作用。激活的信号通路进一步诱导角质形成细胞、树突细胞、Thl7、γδT细胞、中性粒细胞等产生一系列炎性因子（如白细胞介素1、23、17，干扰素α等），这些炎性因子对银屑病样皮损的形成起到重要的作用。
Imiquimod is one of the medicines for the treatment of human papillomavirus infection. Since it was found to induce psoriasis-like skin lesions and aggravate psoriasis in patients during clinical use, it has been widely applied to studies on the pathogenesis of and treatment targets in psoriasis. Imiquimod-induced psoriasis-like mouse model is easy to operate and establish. After treatment with imiquimod, several signaling pathways in mice are activated, including the Toll- like receptor signaling pathway, and some signaling pathways show synergetic effects. Activated signaling pathways can further induce keratinocytes, dentritic cells, T helper 17 （Thl7）ceils, γδT ceils and neutrophils to produce a series of inflammatory factors, such as interleukin （IL）- 1, -23, -17 and interferon-α. These inflammatory factors play important roles in the formation of psoriasis-like skin lesions.
出处
《国际皮肤性病学杂志》
2017年第6期345-348,共4页
International Journal of Dermatology and Venereology
