慢性阻塞性肺疾病已成为中国乃至全球重要的公共卫生问题。目前认为免疫功能紊乱引起的慢性炎性反应是其主要的发病机制之一。2型固有淋巴细胞能快速释放II型细胞因子、调控适应性免疫参与呼吸道炎症反应，Notch1-GATA3信号途径能调节免疫细胞的发育和分化，但其调控适应性免疫参与COPD炎性反应的作用机制尚不明确。本课题使用流式检测肺脾气虚型COPD稳定期和急性加重期患者外周血中ILC2s和naïve CD4+T细胞的变化，基因芯片分析患者免疫细胞Notch1-GATA3关键基因的变化情况；结合动物实验分析干扰Notch1-GATA3后ILC2s对naïve CD4+T的作用。旨在探讨ILC2s参与肺脾气虚型COPD的免疫过程，了解ILC2s与naïve CD4+T细胞相互调控的作用机制，从固有-适应性免疫新对话角度揭示ILC2s对COPD的免疫作用机制，以期为COPD治疗药物的研发提供潜在靶点

Chronic Obstructive Pulmonary Disease is a public health issue in China and even in the whole world. Chronic inflammatory response is one of the main pathogenesis of COPD. 2 Innate Lymphoid Cells involved in respiratory inflammation by regulating the adaptive immunity and release type II cytokines.Notch1-GATA3 signaling pathway is involved in COPD disease physiological process, and adjusts the immune cells and affects the development and differentiation. This subject decide to analyze the difference of ILC2s and n peripheral blood in lung spleen-deficiency type patients with acute exacerbation phase and stable phase, and analyze the changes of Notch1-GATA3 signal pathways. Then analyze the interaction between ILC2s CD4+T cells after the interference of Notch1-GATA3 Signal Pathway, Preliminary discussion the mechanism research of ILC2s regulate adaptive immune system by the Notch1-GATA3 signaling pathway in lung and spleen deficiency COPD, understand the role of ILC2s and CD4+T cells in COPD disease. From the perspective of natural immune adaptive immunity new dialogue reveals ILC2s immune mechanism of COPD, also hope to provide a potential targets for COPD treatment drug research and development. The research will provide new method and target spot for COPD with TCM and its results have important theoretical significance and potential application prospects.