In α-DEC-ESAT-treated animals, we observed that at 14 days post-infection, and in contrast with results obtained in α-DEC-ESAT-untreated mice, the lungs had a high percentage of ESAT-6-specific IFN-γ-producing T cells, elevated in vivo target cell killing, and a considerable reduction of lung bacterial burden. The gene discussed is IFNG; the disease is infection.