IFNG and respiratory tract infectious disorder: In a chronic respiratory infection model in mice, lung macrophages cycle from a resting state to an M2 phenotype, that corresponds with initial proliferation of C. neoformans in the lungs, followed by an M1 phenotype, that correlates to a period of fungal clearance, and then back to a resting state; this cycling could be simulated in vitro by modifying the cytokine environment with either IFNγ (M1) or IL-4 (M2) [184,185].