巨噬细胞的自噬及其在抗结核分枝杆菌感染中的作用

Autophagy in macrophage and its role in the resistance to intracellular Mycobacterium tuberculosis infection

白噬是广泛存在于真核细胞内的一种溶酶体依赖性的自降解途径，可通过降解长寿蛋白和受损细胞器维持细胞内的平衡。近年来的研究发现，巨噬细胞的自噬还是固有免疫和适应性免疫的重要组成部分，可参与胞内感染病原体的清除。目前已发现有多种途径参与自噬的诱导和调节。在感染的巨噬细胞内，诱导自噬的发生能促进吞噬体和溶酶体的融合，抑制胞内结核分枝杆菌（Mtb）的存活。但同时Mtb也可通过某些机制抑制巨噬细胞自噬的发生以逃避巨噬细胞的杀伤，进而长期持留于巨噬细胞内。深入了解巨噬细胞自噬与胞内Mtb相互作用的机制，有助于人类更好的预防和控制结核病。

Autophagy, a lysosome-dependent self-degradation pathway, that generally exists in eukaryotic cells, can maintain cellular homeostasis by degrading long-lived proteins and damaged organelles. Re-ently, autophagy has also been found to play important roles in both natural and adaptive immunity. One mani- fested example is that autophagy in macrophage was associated with the resistance to intracellular pathogens. Many mechanisms and pathways were found to be involved in the induction and regulation of autophagy. In macrophage, induction of autophagy could decrease the survival of intracellular Mtb by promoting the fusion of phagosome and lysosome. However, Mtb has its strategies to restrain the autophagy in macrophage, thereby to escape from being killed and persist in macrophage. Illuminating the interplay between autophagy in macrophage and Mtb could benefit the control of tuberculosis.