Autophagy and Mycobacterium Tuberculosis: the role of autophagy in antimicrobial immunity and therapy

Tuberculosis (TB) remains one of the most severe infectious diseases worldwide, posing a persistent and increasingly serious threat to global public health. Cellular autophagy, a highly conserved innate immune mechanism, plays a crucial role in the elimination of intracellular pathogens, regulation of immune responses, and maintenance of cellular homeostasis, making it a key focus in TB research. This review systematically summarizes the types and regulatory mechanisms of autophagy, as well as its interactions with <i>Mycobacterium tuberculosis</i> (<i>M. tb</i>), and explores the potential applications of autophagy-based host-directed therapeutic strategies. It also addresses the major challenges in current research, including the complex mechanisms by which <i>M. tb</i> evades autophagy, the selectivity and safety concerns of autophagy modulators, and the technical barriers to clinical translation. Growing evidence suggests that autophagy has emerged as a promising therapeutic target for TB, and autophagy modulators may serve as effective adjunctive therapies. Future research should further elucidate the interactions between autophagy and immunometabolic pathways, optimize the targeted delivery of autophagy activators, and verify their efficacy and safety through systematic clinical studies, thereby providing new theoretical foundations and therapeutic strategies for TB prevention and treatment.