With a view to determining whether failure of mice to resolve Mycobacterium tuberculosis (Mtb) infection is a consequence of downregulation of T helper 1 (Th1) immunity by interleukin (IL)‐10, mice deleted of the gene for IL‐10 were compared with wild‐type (WT) mice in terms of their ability to make IL‐10 mRNA, generate Th1‐mediated immunity [as measured by synthesis of mRNA for interferon‐γ (IFN‐γ)], IL‐12p40 and inducible nitric oxide synthase (iNOS), and to control lung infection. It was found that the response of WT mice to infection included a substantial and sustained increase in IL‐10 mRNA synthesis in the lungs. A Th1 response in the lungs of WT and IL‐10^−/− mice was evidenced by a large and sustained increase in the synthesis of mRNA for IFN‐γ, IL‐12p40 and iNOS, with somewhat higher levels of these mRNA species being made in the lungs of IL‐10^−/− mice, particularly at an early stage of infection. However, IL‐10^−/− mice were no more capable than WT mice at combating infection.