结核病是结核分枝杆菌(Mtb)引起的传染病。Mtb感染宿主后在巨噬细胞内存活，其存活与氨基酸转运有关。研究表明苏氨酸转运蛋白与大肠杆菌存活相关。苏氨酸转运蛋白与Mtb跨膜蛋白Rv3737高度同源，但Rv3737是否参与Mtb在巨噬细胞内存活目前未见报道。我们前期研究表明Mtb标准菌株H37Rv感染巨噬细胞后Rv3737表达增高，且与Mtb复制有关；且Rv3737在肺结核患者Mtb临床分离株中高表达，与肺部病变程度相关。本研究拟通过基因敲除、回补技术及苏氨酸转运率观察Rv3737对Mtb在巨噬细胞内存活的影响，从mRNA及蛋白质水平检测Mtb感染巨噬细胞炎症因子的释放，用蛋白质印迹、CO-IP、激光共聚焦等方法了解Rv3737调控炎症及自噬通路对Mtb在巨噬细胞内存活的影响，探讨Rv3737是否通过调节苏氨酸转运影响巨噬细胞炎症免疫应答及自噬，从而影响Mtb在巨噬细胞内的存活机制，了解Mtb致病机理，为新药研发提供靶点。

Mycobacterium tuberculosis (Mtb), the causative agent of human tuberculosis is one of the most widely spread human pathogens. Mtb infected host，then survived in macrophages for a long time, mycobacterial survival was associated with amino acid transport. Studies showed that threonine transporters are associated with the survival of E.coli. The E.coli threonine transporter is highly homologous with Mtb transmembrane protein Rv3737, but whether Rv3737 is involved in Mtb survival in macrophages, which is unclear. Our previous study showed that the expression of Rv3737 was increased in H37Rv infected macrophages, which was related to Mtb replication in macrophages. Furthermore the expression of Rv3737 was highly increased in the clinical isolates from patients with tuberculosis, which was correlated with the degree of pulmonary lesions. Our study observed that whether Rv3737 regulate the mycobacterium survival in the infected macrophages through knockout, complemented Rv3737 in the H37Rv and threonine transfer rate, detecting the expression of inflammatory cytokines in mycobacterium infected macrophages, to understand whther Rv3737 regulate inflammation and autophagy pathways for Mtb in macrophage survival, in order to investigate that whether Rv3737 regulated macrophages inflammatory immune response and autophagy through threonine transhipment,furthermore, which affect Mtb survival and mechanismin in macrophages, to understand Mtb pathogenesis, provide targets for new drug research and development.