目前认为银屑病是一由免疫应答过程异常引发的慢性复发性炎症性疾病，发病机制未明。课题组近年来开展银屑病代谢组学及相关研究，首次报道了银屑病患者血清乳酸水平呈显著增加。British Journal of Dermatology为此发表述评，指出我们的研究提示了乳酸是银屑病发生发展中应该引起重视的必要环节。我们推测乳酸对IL-23/IL-17轴相关免疫调节的影响很可能是联系代谢组学与免疫学的桥梁；代谢紊乱与免疫紊乱密切相关，由此引起或促进银屑病发生发展。因此，本项目主要研究内容是（1）应用靶标代谢组学技术量化人银屑病皮损与正常皮肤乳酸及相关代谢物的差异（2）通过体外乳酸刺激银屑病相关抗原递呈细胞（APC）和效应T细胞，研究乳酸对银屑病中IL-23/IL-17轴的活化机制（3）通过构建银屑病鼠模型，验证乳酸对银屑病发病的影响。本研究将为银屑病的发生发展提供线索，为揭示银屑病的发病机制提供依据。

The pathogenesis of psoriasis remains unclear till now. Currently psoriasis is regarded as a chronic recurrent inflammatory disease caused by abnormal immune response process. In recent years, our group focused on the metabolomics and related studies of psoriasis and reported for the first time that glycolytic activity was significantly increased as revealed by high lactic acid levels in psoriasis patients, as commented in the editorial published in the British Journal of Dermatology (BJD). Our hypothesis is that lactic acid could be a potential link between metabolomics and immunology of psoriasis providing that the IL-23/IL-17 axis related immune regulation is affected by lactic acid. Metabolic disorders are closely related to immune disorders, which may cause or promote the occurrence and development of psoriasis. In order to further explore the relationship between lactic acid and psoriasis, the main research contents of this project are: (1) Quantification of lactic acid and related metabolites in human psoriatic skin and healthy skin by using the technique of target metabolomics; (2) Study on the activation mechanism of lactic acid on IL-23/IL-17 axis in psoriasis by in vitro stimulation of APC cells and T cells; (3) Validation the effect of lactic acid on the pathogenesis of psoriasis by constructing animal model of psoriasis. This study will provide clues for the occurrence and development of psoriasis, and give evidence for revealing the pathogenesis of psoriasis.