Nonetheless, depleting CD4+ T cells or blocking IL-17A did not rescue the increased neutrophil accumulation in the lungs of M. tuberculosis-infected Atg5fl/fl-LysM-Cre mice at 14 dpi, suggesting that the hyper-inflammatory responses from infected autophagy-deficient macrophages and DCs is sufficient to recruit excessive neutrophils early during infection. This evidence concerns the gene IL17A and infection.