Increased interleukin-10 expression is not responsible for failure of T helper 1 immunity to resolve airborne Mycobacterium tuberculosis infection in mice


Robert J. North, The Trudeau Institute, 100 Algonquin Ave, Saranac Lake, NY 12983, USA. E-mail:


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.