[Research progress on miRNA-regulated macrophage polarization and autophagy in immune escape by Mycobacterium tuberculosis].

Latent tuberculosis infection (LTBI), characterized by the host immune system's ability to contain Mycobacterium tuberculosis (MTB) proliferation while failing to fully eliminate the pathogen, is a critical stage in tuberculosis prevention and control. Macrophages and alveolar epithelial cells together constitute the first line of defense. Following infection, MTB triggers a series of responses in which miRNAs, in concert with other biomolecules, coordinately regulate macrophage polarization, autophagic activity, the key metabolic pathways of autophagy, and the inflammatory response of host macrophages. This review summarizes the core mechanisms by which MTB exploits miRNAs to regulate host macrophage polarization, autophagy, and immunity, encompassing both the specific pathways that promote LTBI through autophagy inhibition and the induction of immunosuppressive phenotypes, and the shared mechanisms by which MTB disrupts host antimicrobial immunity during active tuberculosis.