01869nas a2200229   4500000000100000008004100001260001200042653001400054653002800068653003200096653001700128653003300145653001300178100001300191700001000204245011900214856008100333300001100414490000700425520119300432022001401625       2020                            d  c01/202010aautophagy10ahost-directed therapies10ahost–microbe interactions10amycobacteria10anon-tuberculous mycobacteria10avaccines1 aStrong E1 aLee S00aTargeting Autophagy as a Strategy for Developing New Vaccines and Host-Directed Therapeutics Against Mycobacteria.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7840607/pdf/fmicb-11-614313.pdf  a6143130 v113 a<p>Mycobacterial disease is an immense burden worldwide. This disease group includes tuberculosis, leprosy (Hansen's disease), Buruli Ulcer, and non-tuberculous mycobacterial (NTM) disease. The burden of NTM disease, both pulmonary and ulcerative, is drastically escalating globally, especially in developed countries such as America and Australia. Mycobacteria's ability to inhibit or evade the host immune system has contributed significantly to its continued prevalence. Pre-clinical studies have highlighted promising candidates that enhance endogenous pathways and/or limit destructive host responses. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents, small molecules, and autophagy-activating vaccines may be beneficial in restricting intracellular mycobacterial infection, even with multidrug-resistant strains. This review will examine how mycobacteria evade autophagy and discusses how autophagy could be exploited to design novel TB treatment strategies, such as host-directed therapeutics and vaccines, against  and NTMs.</p>  a1664-302X