Tourette综合征（TS）的治疗难点在于复发，中医认为其病机为“外风引动内风”；结合先期研究成果，提出复发病机的神经免疫机制假说：在外源性致病原触发下（外风），失衡的外周细胞因子启动JAK2/STAT3信号通路（引动），激活小胶质细胞，引发神经免疫反应为主的自身免疫失衡（内风），促成TS的发生发展。将建立经典动物及原代小胶质细胞模型，运用免疫荧光染色、Western-Blot等技术，观察各模型在“外风”LPS/RSV刺激前后信号通路相关蛋白、小胶质细胞活性（形态、CD11b表达）和炎性因子变化；构建JAK2/STAT3信号通路高表达/沉默的小胶质细胞模型，考察以上指标变化，进一步证实此通路对小胶质细胞活性的调节作用；同时予中药干预，从药物效应反推的角度证实假说并探索作用靶点。本项目将TS的机制研究拓展到中枢效应细胞领域，为促发新的治疗策略及新药开发提供更多可能。

The difficulty of treatment of Tourette syndrome (TS) are recurrence and complication. The pathogenesis of TS form Traditional Chinese Medicine is “external wind stirs internal wind” . Combined with our previous research, a hypothesis was established: Nerve-immunity axis. Exogenous pathogenic (LPS and RSV, “external wind”) caused the imbalance of peripheral cytokines, and cytokines activated JAK2/STAT3 pathway (“stirs”), and further activated microglia, which resulted in imbalance of nerve-immunity axis (“internal wind”). The above process caused the development of TS. We used classical animal models and primary microglia cell model to investigate the pathogenesis of TS by Western, immunofluorescence and cell transfection. The protein of signal pathway, the activity of microglia (morphological changes, synaptic protein cd11b expression levels) and cytokines were detected before and after lipopolysaccharide (LPS) or respiratory syncytial virus (RSV) addition. In addition, high expression/silence of JAK2/STAT3 signaling pathway of microglia were established to confirm the role of JAK2/STAT3 signaling pathway in microglia. Meanwhile, we used Traditional Chinese Medicine to confirm our hypothesis. In this study, we used nerve- immunity axis to investigate the pathogenesis of TS. This will be provide new therapy and more drugs for TS.