This underscores that the excessive G-CSF-mediated accumulation of pathogenic immature neutrophils is a specific event observed in TB susceptible male Nox2-/- mice Ultimately, we concluded that upregulated G-CSF is the immunologic trigger for the generation of permissive immature pulmonary neutrophils, which facilitates TB immunopathogenesis and lung hyperinflammation in male Nox2-/- mice (Fig 8). Here, CSF3 is linked to tuberculosis.