咪喹莫特诱导小鼠银屑病样皮损机制的研究进展

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、Th17、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.

Mechanisms of imiquimod-induced psoriasis-like skin lesions in mice

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 (Th17)cells,γδT cells 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.