肺结核病严重威胁我国人口健康和经济社会建设，其主要是由结核分枝杆菌感染肺脏巨噬细胞引起，但目前对其致病机理的研究仍非常有限。我们前期研究发现结核菌感染巨噬细胞可诱导趋化因子MCP-2/CCL8生成，从而募集表达其受体CCR5的CD4+ T 细胞到胸腔积液。另外对中国人群的肺结核病全基因组关联分析发现10 多个未见报道的易感相关基因。进一步的研究发现，这些肺结核病易感相关基因的敲除影响结核菌感染的小鼠的肺部炎症反应。本项目将进一步从分子、细胞、动物模型及临床样本等水平，分析研究结核菌感染对肺部巨噬细胞的功能的影响；以及这些巨噬细胞对其他肺部免疫细胞如T细胞和系统免疫的影响及分子机制；解析确定调控肺部巨噬细胞功能的关键分子及机制。研究结果将不仅加深对结核菌感染对肺脏巨噬细胞功能调控机制的了解，同时还将为提高结核菌免疫诊断和结核病疫苗效果提供可能，具有十分重要的理论意义和实际应用意义。

Tubercuosis (TB) is still a big threat to human health as well economy and society of our country. Pulmonary TB is mainly caused by the infection of macrophages residing in lung tissue with Mycobacterium tuberculosis (Mtb), and lung immune cells have specialized compositions and functions, but the mechanism of how lung-resident macrophage cells are involved in the regulation of pulmonary TB pathogenesis is still unclear. We have performed GWAS analysis of pulmonary TB patients in Chinese population and identified more than 10 TB susceptible genes. Therefore, we are going further to study the mechanism of how lung macrophages including alveolar macrophage, macrophages in TBE or whole are affected by Mtb infection, and how Mtb-infected macrophages regulate the proliferation or differentiation of other cell such as T cells in the lung. Results from our research will not only provide more insights into the characteristic of lung immune system during Mtb infection, but also clarify the novel mechanism of TB pathogensis, and potentiate the development of new TB diagnosis or vaccination strategies..