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Immunization with radiation (γ)-attenuated  Plasmodia  sporozoites (γ-spz) confers sterile and long-lasting immunity against malaria liver-stage infection. In the  P. berghei  γ-spz model, protection is linked to liver CD8 +  T cells that express an effector/memory (T EM ) phenotype, (CD44 hi CD45RB lo CD62L lo  ), and produce IFN-γ. However, neither the antigen presenting cells (APC) that activate these CD8 +  T EM  cells nor the site of their induction have been fully investigated. Because conventional (c)CD8α +  DC (a subset of CD11c +  DC) are considered the major inducers of CD8 +  T cells, in this study we focused primarily on cCD8α +  DC from livers of mice immunized with  Pb  γ-spz and asked whether the cCD8α +  DC might be involved in the activation of CD8 +  T EM  cells. We demonstrate that multiple exposures of mice to  Pb  γ-spz lead to a progressive and nearly concurrent accumulation in the liver but not the spleen of both the CD11c + NK1.1 −  DC and CD8 +  T EM  cells. Upon adoptive transfer, liver CD11c + NK1.1 −  DC from  Pb  γ-spz-immunized mice induced protective immunity against sporozoite challenge. Moreover, in an  in vitro  system, liver cCD8α +  DC induced naïve CD8 +  T cells to express the CD8 +  T EM  phenotype and to secrete IFN-γ. The in vitro induction of functional CD8 +  T EM  cells by cCD8α +  DC was inhibited by anti-MHC class I and anti-IL-12 mAbs. These data suggest that liver cCD8α +  DC present liver-stage antigens to activate CD8 +  T EM  cells, the pre-eminent effectors against pre-erythrocytic malaria. These results provide important implications towards a design of anti-malaria vaccines.

Immunization with Radiation-Attenuated Plasmodium berghei Sporozoites Induces Liver cCD8α+DC that Activate CD8+T Cells against Liver-Stage Malaria