At initial stages of infection, ARG1 activity favors survival of the pathogen by dampening macrophage immunity through substrate competition with iNOS/NOS2; during the chronic stage of infection, when prolonged hyperinflammation is associated with exacerbation of lung immunopathology, ARG1 contributes to control of infection by modulating the development of lung immunopathology through repressing T cell proliferation, as seen in M. tuberculosis-infected Nos2-deficient mice (96). Here, ARG1 is linked to infection.