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Once there, smoke-expanded pools of alveolar macrophages are paradoxically less effective: phagocytosis, autophagy, antigen presentation, and production of key cytokines such as tumor necrosis factor- (TNF-), interleukin-12 (IL-12), and interferon- (IFN-) are all attenuated, while a shift toward anti-inflammatory M2 phenotypes and smoke-induced metabolic exhaustion enable intracellular survival of the pathogen (Leemans et al., 2005