Mice incapable of making IL-4 or IL-10 display normal resistance to infection with Mycobacterium tuberculosis.
With a view to determining whether production of Th2 cytokines, IL-4 or IL-10, is responsible for the inability of mice to resolve infection with Mycobacterium tuberculosis, mice with targeted disruption of their IL-4 or IL-10 gene were compared with wild-type mice in terms of their ability to defend against an M. tuberculosis infection initiated via the respiratory route. The results show that mice that are unable to make either IL-4 or IL-10 are no more capable than wild-type mice at defending against tuberculosis (TB). Therefore, the results are inconsistent with the proposition that the inadequacy of Th1-mediated anti-tuberculosis immunity is due to its down-regulation by either of these Th2 cytokines.
The Trudeau Institute, Saranac Lake, NY 12983, USA.
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North
D000818:Animals; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis* / Q000235:genetics; D008099:Liver / Q000382:microbiology; D008168:Lung / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009169:Mycobacterium tuberculosis / Q000276:immunology / Q000302:isolation & purification; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000382:microbiology; D018417:Th1 Cells / Q000276:immunology; D014376:Tuberculosis / Q000276:immunology*
D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma