免疫调节失衡是银屑病发病机制的中心环节，多种免疫细胞、细胞因子介导的免疫反应共同调节银屑病的发生发展。外泌体作为细胞间通讯的重要物质，在免疫应答过程中发挥重要作用。Wnt非经典信号通路在银屑病角质形成细胞增殖及慢性炎症反应中发挥重要作用。我们通过miRNA芯片高通量筛查及生物信息学分析等前期研究，发现银屑病患者血清外泌体miR-1305表达水平降低，其调控基因Wnt5a在银屑病患者皮损区高表达。因此我们提出如下科学假说：血清外泌体 miR-1305低表达使Wnt非经典信号通路激活，促进角质形成细胞增殖及诱导Th17细胞分化，导致Treg/Th17调控失衡，细胞因子过度分泌，募集炎症细胞，共同促进银屑病的发生发展。本研究将采用流式细胞仪、透射电镜等实验方法探究miR-1305通过Wnt信号通路调控角质形成细胞增殖和Th17细胞分化的作用机制，为深入研究银屑病发病机制提供理论支持。

Immunomodulatory imbalance palys the central role in the pathogenesis of psoriasis. Inflammatory response mediated by various immune cells and cytokines promotes the occurrence and development of psoriasis. Exosomes play an important role in the process of immune response as an important substance of intercellular communication. Wnt non-classical signaling pathway plays an important role in the proliferation of keratinocytes and chronic inflammatory response in psoriasis. Our previous studies, such as miRNA microarray and bioinformatics analysis, showed that the expression level of miR-1305 in serum exosomes of psoriasis patients decreased, and its regulatory gene Wnt5a was highly expressed in the skin lesions of psoriasis patients. Therefore, we propose the following scientific hypothesis: low expression of serum exosomal miR-1305 activates Wnt non-classical signaling pathway, promotes proliferation of keratinocytes and induces differentiation of Th17 cells, leads to imbalance of Treg/Th17 regulation, over-secretion of cytokines, recruitment of inflammatory cells, and promotes the occurrence and development of psoriasis. In this study, flow cytometry, transmission electron microscopy and other experimental methods will be used to explore the mechanism of miR-1305 regulating keratinocyte proliferation and Th17 cell differentiation through Wnt signaling pathway, and provide theoretical support for further study of the pathogenesis of psoriasis.