| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3415768 | Microbes and Infection | 2007 | 11 Pages |
Vaccine-induced protection against leishmaniasis is largely dependent on cell-mediated type 1 response and IL-12-driven IFN-γ production. Surprisingly, our previous data showed that IL-12/23p40−/− mice could be vaccinated against L. amazonensis and were able to produce limited amounts of IFN-γ. Since the role of CD8+T in immunization against L. amazonensis is obscure, the aim of this study was to evaluate the effects of CD8+ cells in protection against L. amazonensis in IL-12/23p40−/− mice. In order to deplete CD8+ cells, one group of vaccinated animals was treated with anti-CD8 mAb. Infection was followed for 8 weeks. The vaccinated CD8+-depleted group developed smaller lesions than the non-depleted group. CD8 depletion did not affect tissue parasitism or antibody response against the parasite, and treated animals displayed milder inflammation and better tissue integrity. IFN-γ production in spleen and draining lymph node was impaired in the depleted group, suggesting that CD8+ cells produced this cytokine in IL-12-independent vaccination. Such results suggest that this T cell subset contributes to augmented pathology in IL12/23p40−/− mice vaccinated and challenged with L. amazonensis. Although these cells could produce some IFN-γ the in the absence of IL-12, they do not affect the parasite tissue load.
