青蒿琥酯（ART）具有直接抑制肿瘤细胞作用，但对肿瘤免疫微环境的作用所知甚少。CD8+T是介导抗肿瘤免疫的效应细胞，最新研究显示CD39可作为肿瘤特异性CD8+T细胞的有效标志物。我们发现ART可体外选择性诱导肺癌患者CD8+CD39+T细胞增多、NF-κB核转位及体外杀伤肺癌细胞效应，biacore实验显示ART与盘状球蛋白JUP相互作用。据此，推测ART结合JUP活化NF-κB通路上调CD39+CD8+T。本项目拟通过体外实验明确ART结合JUP诱导NF-κB通路活化的分子机制；通过小鼠肺癌模型明确ART体内活化CD39+CD8+T及抗肿瘤作用；通过临床标本检测，分析ART作用靶点与肺癌疗效、转归的相关性，以期为临床预后提供新指标。本研究将为肺癌CD8+CD39+T细胞活化提供新机制，为疾病干预提供新思路。

Artesunate (ART) can directly inhibit tumor cells, but little is known about the role in tumor immune microenvironment. CD8+T cell is the effect cell against tumor, the last studies show CD39 can be used as an effective marker for tumor-specific CD8+T. We found that ART can selectively induce the proliferation of CD8 + CD39 + T cells, the nuclear translocation of NF-kappa B and the cytotoxic effect of ART on lung cancer cells in vitro. Additionally, biacore assay showed that ART interacted with Junction Plakoglobin (JUP) directly. Based on that data, we speculate that ART up-regulates CD39+CD8+T through NF-κB pathway by interacting JUP. This project aims to elucidate of activation of NF-kappa B pathway induced by ART combined with JUP through in vitro experiments, to clarify the role of ART in CD39+CD8+T activation and tumor inhibition through the mouse lung cancer model, to analyze the relationship between ART targets and the therapeutic effect and prognosis of lung cancer through the detection of clinical specimens, in order to provide new biomarkers for clinical prognosis. This study will provide a mechanism for the activation of CD39+CD8+T in lung cancer and a new idea for disease intervention.