In contrast, IFN-γR-deficient mice reconstituted with IFN-γR-deficient bone marrow lost a significant amount of body weight (Fig 7A, left), eventually succumbed to infection with similar kinetics to IFN-γ-deficient controls (Fig 7B), had bacteria in the spleen, lung, and kidneys (Fig 7C), and had delayed resolution of FRT infection (Fig 7D). Here, IFNGR1 is linked to infection.