Host–mycobacteria molecular axes that connect the sections of this review Pattern recognition signaling—TLR2, NOD2, C-type lectins (mannose receptor, DC-SIGN, Mincle/MCL, Dectin-2), cGAS–STING, and the NLRP3 inflammasome. Phagosome subversion—arrest of phagosome maturation and ESX-1-mediated phagosomal membrane damage. Macrophage immunometabolism—the glycolytic (Warburg-like) switch, foamy-macrophage formation, and the apoptosis-versus-necrosis decision. Phosphoantigen sensing—HMBPP/IPP through the BTN3A1/BTN2A1–Vγ9Vδ2 axis. γδ T cell effectors—IFN-γ/TNF activation of macrophages and granulysin-mediated anti-mycobacterial activity. Damage axes in COPD—the IL-17A–G-CSF–neutrophil axis and protease-driven injury (neutrophil elastase, MMP-12, NETs). BCG-induced trained immunity—NOD2-dependent epigenetic and metabolic reprogramming of myeloid and innate-like cells.