系统性红斑狼疮（SLE）是常见的自身免疫性疾病，辅助性T细胞17（Th17）和调节性T细胞（Treg）失衡是导致SLE发病的关键因素之一，但造成其失衡的机制有待明确。我们前期发现芳香烃受体（AhR）可导致SLE疾病Th17/Treg失衡。课题组预实验证实Hippo-TAZ信号通路的关键分子与AhR存在相互作用关系，并且其参与SLE发病。据此，我们提出科学假说：AhR经Hippo-TAZ信号通路诱导Th17/Treg失衡进而导致SLE发病。本项目拟通过SLE患者-体外细胞-模型动物三个层面，采用质谱流式细胞、免疫共沉淀和生物信息学等技术，证明AhR经Hippo-TAZ信号通路诱导Th17/Treg失衡促进SLE发病的作用机制，并明确AhR和Hippo-TAZ信号通路的关键分子在SLE疾病早期诊断中的价值，为完善SLE发病机制提供理论依据，为提高SLE早期诊断能力提供潜在的分子标志物。

Systemic lupus erythematosus (SLE) is a common autoimmune disease. The imbalance of helper T cell 17 (Th17) and regulatory T cell (Treg) is one of the key factors for generating the pathogenesis of SLE. However, the mechanisms leading to the imbalances are remain unclear. We have previously demonstrated that aryl hydrocarbon receptor (AhR) can cause the imbalance of Th17/Treg in SLE disease. Our preliminary experiment showed that the key molecules of Hippo-TAZ signaling pathway could interact with AhR and participate in the pathogenesis of SLE. Based on these, we propose a scientific hypothesis: AhR induces the imbalance of Th17/Treg through Hippo-TAZ signaling pathway and leads to the pathogenesis of SLE. With SLE patients, cell experiment in vitro and SLE model mice, we reveal the mechanisms of AhR mediates Th17/Treg imbalance in SLE, and to identify the molecular biomarkers value of AhR and Hippo-TAZ signaling pathway related molecules in the early diagnosis of SLE by mass spectrometry, co-immunoprecipitation and bioinformatics. Our study is expected to provide a theoretical basis for perfecting the pathogenesis of SLE, and to provide potential molecular biomarkers for improving the early diagnosis of SLE.