Abstract
Abstract IL-17 family cytokine is comprised of six members, IL-17A to IL-17F. Recent studies using cytokine- and receptor-deficient mice showed that IL-17A and IL-17F were required for responses to extracellular bacterium K. pneumonia in the lungs and C. rodentium in the colon, respectively. However, the involvement of IL-17A and IL-17F in protective immunity was well not clearly demonstrated in mycobacterial infected lung. In this study, we analyzed role of IL-17A and IL-17F in host defense against chronically infected M. tuberculosis. using IL-17A- and IL-17F-KO mice. The IL-17A-KO mice showed significantly decreased survival rates compared with the wild-type (WT) mice during 250-day observation period. In contrast, survival rate of the IL-17F-KO mice were similar to that of the WT mice. Bacterial burdens of various organs of the IL-17F-KO mice on the day 250 were nearly the same as that in the WT mice. In the infected lungs, the IL-17A-KO mice produced less IFN-γ, TNF and IL-6 in comparison to those from the WT mice, while cytokine production of the IL-17F-KO mice were similar to that of the WT mice. This result indicated that the generation of Th1 cells was impaired in the IL-17A-KO mice but not in the IL-17F-KO mice infected with M. tuberculosis. These data strongly support the notion that the lack of IL-17F neither suppress nor enhances protective immunity in the lung after mycobacterial infection.
Published Version
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