结核分枝杆菌免疫逃逸机制的研究进展

结核分枝杆菌是一种烈性、强毒、传染性病原菌。由其引发的结核病极难治愈，普通的抗生素药物对其根本不起作用。究其原因是该菌通过一系列目前仍尚未阐明的逃逸机制逃脱了巨噬细胞溶酶体对其的融合杀伤作用，因而得以存活并寄生在巨噬细胞内的吞噬体中。对此，近年来发表了一系列极有价值的研究成果，主要集中在可溶性N-乙基顺丁希二酰亚胺敏感因子连接蛋白受体（SNARE）融合核心复合体的形成，Rab7、Rab5及其效应蛋白EEA-1在晚内体成熟中的作用以及自噬在免疫逃逸机制中的作用等几个方面，这对于进一步丰富和阐明结核分枝杆菌的免疫逃逸机制理论具有重要意义。

Advance of study on the immune escape mechanism of Mycobacteria

Mycobacterium is a kind of spirited, poisonous, infectious pathogens. Tuberculosis caused by mycobacteria is extremely difficult to cure and these commonused antibiotic drugs are not clinically effective.The reason could be explained as follows: the pathogens escape from the fusion destruction of macrophage lysosomes through a series of unclear immune escape mechanism, and then survive and be parasitic in the phagosome of macrophage. A series of valuable achievements which mainly focus on the formation of SNARE complex, the role of Rab7, Rab5 and its effect protein EEA-1 in the maturation of late endosome, the role of autophagy in the immune escape mechanism have been published these year. It is important to clarify the role of Mycobacteria in immune escape.