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Autophagy is an important innate immune defense mechanism that controls <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) growth inside macrophages. Autophagy machinery targets <i>Mtb</i>-containing phagosomes via xenophagy after damage to the phagosomal membrane due to the Type VII secretion system Esx-1 or via LC3-associated phagocytosis without phagosomal damage. Conversely, <i>Mtb</i> restricts autophagy-related pathways via the production of various bacterial protein factors. Although bacterial lipids are known to play strategic functions in <i>Mtb</i> pathogenesis, their role in autophagy manipulation remains largely unexplored. Here, we report that the lipid virulence factors sulfoglycolipids (SLs) and phthiocerol dimycocerosates (DIMs) control autophagy-related pathways through distinct mechanisms in human macrophages. Using knock-out and knock-in mutants of <i>Mtb</i> and <i>Mycobacterium </i><i>bovis</i> BCG (Bacille Calmette Guerin) and purified lipids, we found that (i) <i>Mtb</i> mutants with DIM and SL deficiencies promoted functional autophagy via an MyD88-dependent and phagosomal damage-independent pathway in human macrophages; (ii) SLs limited this pathway by acting as TLR2 antagonists; (iii) DIMs prevented phagosomal damage-independent autophagy while promoting Esx-1-dependent xenophagy; (iv) and DIMs, but not SLs, limited the acidification of LC3-positive <i>Mtb</i> compartments. In total, our study reveals an unexpected and intricate role for <i>Mtb</i><i> </i>lipid virulence factors in controlling autophagy-related pathways in human macrophages, thus providing further insight into the autophagy manipulation tactics deployed by intracellular bacterial pathogens.