CSF3 and infection: IL-17 has been implicated as a pivotal regulator of G-CSF expression during emergency granulopoiesis and basal neutrophilia.96 IL-17 was also found to be critical to G-CSF-mediated neutrophil responses during infection, as mice lacking IL-17A receptors exhibited increased susceptibility to Klebsiella pneumoniae due to decreased production of G-CSF at the site of infection.97