Furthermore, in vivo neutralization of IL-6, IL-1α, and IL-1β also aggravated immature neutrophil-mediated TB pathogenesis and lung hyperinflammation in Nox2-/- mice, although IL-1 is reported to be crucial for mediating neutrophilic inflammation in NOX2-deficient conditions [12,36,37,44] (S9 Fig). This evidence concerns the gene IL1A and tuberculosis.