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The Journal of Immunology, Vol 158, Issue 1 315-321, Copyright © 1997 by American Association of Immunologists

ARTICLES

T cell-derived IL-10 antagonizes macrophage function in mycobacterial infection

PJ Murray, L Wang, C Onufryk, RI Tepper and RA Young
Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.

Pathogenic mycobacteria survive within macrophages despite T cell responses that activate host defenses against most pathogens. Among cytokines produced by T cells, IL-10 is known to negatively regulate Th1 cells as well as macrophages. IL-10 has been shown to inhibit the anti-mycobacterial activity of macrophages in vitro and could account for the ability of mycobacteria to survive intracellularly. To test the inhibitory functions of IL-10 in vivo, transgenic mice that secrete IL- 10 from the T cell compartment were constructed and infected with Calmette-Guerin bacillus (Mycobacterium bovis). These mice were unable to clear the infection and developed large bacterial burdens. Nonetheless, their T cells produced abundant amounts of IFN-gamma and IL-2 in response to Ag challenge. These results indicate that the presence of excess IL-10 had little, if any, effect on T cell function or development during the immune response to Calmette-Guerin bacillus. Rather, the data suggest that IL-10 helps maintain mycobacterial infections by acting primarily at the level of the macrophage, overriding anti-mycobacterial signals delivered by IFN-gamma.


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