The immune response toMycobacterium tuberculosisinfection determines tuberculosis disease outcomes, yet we have an incomplete understanding of what immune factors contribute to a protective immune response. Neutrophilic inflammation has been associated with poor disease prognosis in humans and in animal models duringM.tuberculosisinfection and, therefore, must be tightly regulated. ATG5 is an essential autophagy protein that is required in innate immune cells to control neutrophil-dominated inflammation and promote survival duringM.tuberculosisinfection; however, the mechanistic basis for how ATG5 regulates neutrophil recruitment is unknown. To interrogate what innate immune cells require ATG5 to control neutrophil recruitment duringM.tuberculosisinfection, we used different mouse strains that conditionally deleteAtg5in specific cell types. We found that ATG5 is required in CD11c+cells (lung macrophages and dendritic cells) to control the production of proinflammatory cytokines and chemokines duringM.tuberculosisinfection, which would otherwise promote neutrophil recruitment. This role for ATG5 is autophagy dependent, but independent of mitophagy, LC3-associated phagocytosis, and inflammasome activation, which are the most well-characterized ways that autophagy proteins regulate inflammation. In addition to the increased proinflammatory cytokine production from macrophages duringM.tuberculosisinfection, loss of ATG5 in innate immune cells also results in an early induction of TH17 responses. Despite prior published in vitro cell culture experiments supporting a role for autophagy in controllingM.tuberculosisreplication in macrophages, the effects of autophagy on inflammatory responses occur without changes inM.tuberculosisburden in macrophages. These findings reveal new roles for autophagy proteins in lung resident macrophages and dendritic cells that are required to suppress inflammatory responses that are associated with poor control ofM.tuberculosisinfection.