The roles of IL-12 and IL-23 in CD8 T cell-mediated immunity against Listeria monocytogenes: Insights from a DC vaccination model |
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Authors: | Curtis J Henry Jason M Grayson Latoya M Mitchell Marlena M Westcott Elizabeth M Hiltbold |
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Institution: | a Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA b Department of Biochemistry and Molecular Genetics, University of Colorado Denver, Aurora, CO 88010, USA c Integrated Department of Immunology, National Jewish Health, Denver, CO 80206, USA d Department of Microbiology, University of Alabama - Birmingham, Birmingham, AL 35243, USA |
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Abstract: | Listeria monocytogenes infection induces a strong inflammatory response characterized by the production of IL-12 and IFN-γ and protective immunity against this pathogen is dependent on CD8+ T cells (CTL). Recent studies have suggested that these inflammatory cytokines affect the rate of memory CD8+ T cell generation as well as the number of short-lived effector cells generated. The role of the closely related cytokine, IL-23, in this response has not been examined. We hypothesized that IL-12 and IL-23 produced by dendritic cells collectively enhance the generation and function of memory cells. To test this hypothesis, we employed a DC vaccination approach. Mice lacking IL-12 and IL-23 were vaccinated with wild-type (WT), IL-12−/−, or IL-12/23−/− DC and protection to Lm was monitored. Mice vaccinated with WT and IL-12−/− DC were resistant to lethal challenge with Lm. Surprisingly, mice vaccinated with IL-12/23−/− DC exhibited significantly reduced protection when challenged. Protection correlated with the relative size of the memory pools generated. In summary, these data indicate that IL-23 can partially compensate for the lack of IL-12 in the generation protective immunity against Lm. |
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Keywords: | Inflammatory cytokines Interleukin-12 and interleukin-23 Dendritic cells Cytolytic T cells Listeria Protective immunity |
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