摘要: Macrophages are first-line responders against microbes. The success of Mycobacterium tuberculosis (Mtb) rests upon its ability to convert these antimicrobial cells into a permissive cellular niche. This is remarkable accomplishment, as the arsenal macrophages extensive. Normally bacteria delivered an acidic, degradative lysosome through one several trafficking pathways, including LC3-associated phagocytosis (LAP) and autophagy. Once phagocytozed, bacilli subjected reactive oxygen nitrogen species, they induce expression proinflammatory cytokines, which serve augment host responses. However, Mtb hijacks defense mechanisms, manipulating trafficking, innate immune responses, cell death pathways benefit. complex series measures countermeasures between pathogen ultimately determines outcome infection. In this review, we focus on diverse effectors that uses in multipronged effort subvert responses macrophages. We highlight recent advances understanding molecular interface Mtb-macrophage interaction.