银屑病是皮肤科常见的慢性炎症性自身免疫性疾病，确切的发病机制尚不明确。已证实IL-23/IL-17轴是银屑病发生发展的重要介导因子，因此已成为潜在的药物治疗靶点。双氢青蒿素(dihydroartemisinin，DHA) 是青蒿素类化合物的主要活性代谢物，研究发现DHA对治疗自身免疫性疾病疗效肯定，且无明显毒副作用。我们的前期研究发现，DHA可改善咪喹莫特所致小鼠银屑病样皮肤炎症。本研究拟采用不同刺激剂活化小鼠树突状细胞及CD4+T细胞，验证DHA对IL-23/IL-17轴与Th17极化的调节作用；建立咪喹莫特诱导的银屑病模型，证实DHA基于IL-23/IL-17信号轴与Th17极化的调节作用抑制银屑病演进；采用银屑病患者外周血验证DHA对促炎症因子的抑制作用及对Th17细胞分化的影响。本研究将阐明DHA对银屑病的免疫调节作用及机制，为银屑病提供新的治疗靶点。

Psoriasis is an autoimmune-ralated chronic inflammatory skin disease. Recently study indicated that IL-23/IL-17 axis plays a significant role in psoriasis. Therefore, IL-23/IL-17 axis has become a potential drug treatment target. Dihydroartemisinin (DHA) is the main active metabolite of artemisinin compounds. Some studies have found that DHA has a potent effect on the treatment of autoimmune diseases without obvious toxic and side effects. Our previous study found that DHA improved mice psoriasis-like skin inflammation, induced by imiquimod. In this study, different stimulants will be used to activate mouse dendritic cells and CD4+T cells to verify the regulatory effect of DHA on IL-23/IL-17 axis and Th17 polarization. Imiquimod-induced mouse psoriasis model will be established to confirm that DHA inhibite psoriasis progression based on IL-23/IL-17 axis and Th17 polarization. Peripheral blood of patients with psoriasis will be used to verify the inhibitory effect of DHA on proinflammatory cytokines and Th17 cell differentiation. This study will clarify the immunomodulatory effect and mechanism of DHA on psoriasis, and provide a new therapeutic target for psoriasis.