There is evidence in both human and experimental infection caused by Mycobacterium tuberculosis, that immunologic factors influence susceptibility to infection and the progress of the disease. The present study aims to evaluate the role of IFN- g upon inflammatory granulomatous response against M. bovis. To pursue that, C57BL/6 mice lacking the genes for synthesis of IFN- g (IFN- g-/-) and their wild-type counterparts (IFN- g+/+) were intravenously inoculated with M. bovis. The ability of M. bovis to survive and replicate in the liver and lungs was evaluated by counting colony-forming unit (CFU). The histopathological features of granulomatous inflammatory response in the liver and lungs were analyzed during the infection by M. bovis. Granuloma parameters such as, size (sectional area), granuloma volume, volume density, and numerical density were calculated in each point of infection. Bacillary load was higher in both organs of the animals that were IFN- g-/- than in IFN- g+/+ mice. Granulomas were observed in the IFN- g-/- mice after 30 days of infection and were detected earlier in controls (15 days of infection). Hepatic granulomas persisted in the IFN- g-/- mice, but in the IFN- g+/+ mice control of the inflammation. In conclusion, IFN- g influenced the multiplication of M. bovis, as well as modulated the granulomatous inflammation