Mycobacterium tuberculosis (Mtb) is a very successful pathogen, strictly adapted to humans and the cause of tuberculosis. Its success is associated with its ability to inhibit host cell intrinsic immune responses by using an arsenal of virulence factors of different nature. It has evolved to synthesize a series of complex lipids which form an outer membrane and may also be released to enter host cell membranes. In addition, secreted protein effectors of Mtb are entering the host cell cytosol to interact with host cell proteins. We briefly discuss the current model, involving the ESX-1 type seven secretion system and the Mtb lipid phthiocerol dimycoserosate (PDIM), of how Mtb creates pores in the phagosomal membrane to allow Mtb proteins to access to the host cell cytosol. We provide an exhaustive list of Mtb secreted proteins that have effector functions. They modify (mostly inhibit but sometimes activate) host cell pathways such as: phagosome maturation, cell death, cytokine response, xenophagy, reactive oxygen species (ROS) response via NADPH oxidase 2 (NOX2), nitric oxide (NO) response via NO Synthase 2 (NOS2) and antigen presentation via MHC class I and class II molecules. We discuss the host cell targets for each lipid and protein effector and the importance of the Mtb effector for virulence of the bacterium.

结核分枝杆菌（Mtb）是一种非常成功的病原体，严格适应人类和结核病的病因。其成功与通过使用不同性质的毒力因子库抑制宿主细胞固有免疫反应的能力有关。它已经进化为合成一系列复杂的脂质，这些脂质形成外膜，也可能被释放进入宿主细胞膜。另外，Mtb的分泌蛋白效应子进入宿主细胞胞质溶胶，与宿主细胞蛋白相互作用。我们简要讨论了当前模型，涉及ESX-1 7型分泌系统和Mtb脂质苯二酚二羟乙基粘膜酸（PDIM），该模型涉及Mtb如何在吞噬体膜中形成孔以允许Mtb蛋白进入宿主细胞的细胞质。我们提供了具有效应子功能的Mtb分泌蛋白的详尽列表。它们修饰（大部分抑制但有时激活）宿主细胞途径，例如：吞噬体成熟，细胞死亡，细胞因子反应，异种吞噬，通过NADPH氧化酶2（NOX2）产生的活性氧（ROS）反应，通过NO合酶产生的一氧化氮（NO）反应2（NOS2）和通过MHC I类和II类分子进行抗原呈递。我们讨论了每个脂质和蛋白质效应子的宿主细胞靶标以及Mtb效应子对细菌毒性的重要性。