结核病免疫应答中自噬现象的分子机制和意义

The molecular mechanism and significance of autophagy in immune response to mycobacterium tuberculosis

越来越多的证据表明，自噬是结核免疫反应的重要组成部分。自噬可以杀灭结核分枝杆菌、调节促炎细胞因子的分泌、增加抗原递呈功能。自噬与其他抗菌途径如维生素D3、炎性体、泛素系统存在协同作用。另一方面，结核分枝杆菌可以调控巨噬细胞的自噬。目前，自噬已成为临床重要的诊疗靶点。其能诱导自噬的药物，可以作为佐剂治疗耐药性结核；能有效诱导自噬的疫苗，可能提供更好的免疫保护作用。

A growing body of evidence shows that autophagy is an essential component in the immune response to Mycobacterium tuberculosis （Mtb）. Autophagy, a direct mechanism of killing intracellular Mycobacterium tuberculosis, acts as a modulator of proinflammatory cytokine secretion and plays a key role in antigen presentation. Autophagy coordinate with other host immune strategies against mycobacteria, including vitamin D-mediated innate immunity, ubiquitin-and inflammasome-involved pathways. On the other hand, Mtb has its strategies to modulate the autophagy in macrophage. Autophagy offers an attractive therapeutic target. Autophagy-promoting agents could have a clinical application as adjunctive treatment for drug-resistant tuberculosis. Moreover, vaccines which effectively induce autophagy could be more successful in providing better immune protection.