| First Author | Henry CJ | Year | 2010 |
| Journal | Cell Immunol | Volume | 264 |
| Issue | 1 | Pages | 23-31 |
| PubMed ID | 20483409 | Mgi Jnum | J:162123 |
| Mgi Id | MGI:4462770 | Doi | 10.1016/j.cellimm.2010.04.007 |
| Citation | Henry CJ, et al. (2010) The roles of IL-12 and IL-23 in CD8+ T cell-mediated immunity against Listeria monocytogenes: Insights from a DC vaccination model. Cell Immunol 264(1):23-31 |
| abstractText | Listeria monocytogenes infection induces a strong inflammatory response characterized by the production of IL-12 and IFN-gamma 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. |
