Journal
JOURNAL OF IMMUNOLOGY
Volume 169, Issue 11, Pages 6343-6351Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.11.6343
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Funding
- NIAID NIH HHS [AI-41922, AI-44072] Funding Source: Medline
- NIA NIH HHS [AG-06946] Funding Source: Medline
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The production of immunosuppressive cytokines, such as IL-10 and TGF-beta, has been documented in individuals diagnosed with active tuberculosis. In addition, IL-10 production is increased within the lungs of mice that have chronic mycobacterial infection. Therefore, we hypothesized that the down-regulatory properties of IL-10 might contribute to the reactivation of chronic Mycobacterium tuberculosis infection in mice. To determine the influence of IL-10 on the course of infection, transgenic mice producing increased amounts of IL-10 under the control of the IL-2 promotor were infected with M. tuberculosis via the respiratory route. Mice that overexpressed IL-10 showed no increase in susceptibility during the early stages of infection, but during the chronic phase of the infection showed evidence of reactivation tuberculosis with a highly significant increase in bacterial numbers within the lungs. Reactivation was associated with the formation of macrophage-dominated lesions, decreased mRNA production for TNF and IL-12p40, and a decrease in Ag-specific IFN-gamma secretion. These data support the hypothesis that IL-10 plays a pivotal role during the chronic/latent stage of pulmonary tuberculosis, with increased production playing 4 potentially central role in promoting reactivation tuberculosis.
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