Increased interleukin-10 expression is not responsible for failure of T helper 1 immunity to resolve airborne Mycobacterium tuberculosis infection in mice
Article first published online: 20 MAY 2003
Volume 109, Issue 2, pages 295–299, June 2003
How to Cite
Jung, Y.-J., Ryan, L., LaCourse, R. and North, R. J. (2003), Increased interleukin-10 expression is not responsible for failure of T helper 1 immunity to resolve airborne Mycobacterium tuberculosis infection in mice. Immunology, 109: 295–299. doi: 10.1046/j.1365-2567.2003.01645.x
- Issue published online: 20 MAY 2003
- Article first published online: 20 MAY 2003
- Received 29 November 2002; revised 24 February 2003; accepted 11 March 2003.
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.