A schematic view of the immune responses in the BALB/c mice spleens after experimental infection with L. infantum. (A) In the initial stage of infection, parasites from the blood invade macrophages and DCs into the splenic MZ. Also, DCs acquire parasite antigens in the MZ and subsequently migrate to the PALS. (B) DCs produce IL-12 and present parasite antigens to T cells in the PALS. (C) Leishmania-specific T-cells are activated in the PALS but a failure in the specific effector response prevents them from interacting with parasitized host cells in the MZ. Finally, chronicity of infection occurs in the spleen. (D) The kinetics of parasite burden and loss of germinal centers in the spleen after L. infantum infection. The progressive loss of splenic germinal centers increased with time. Thus, in the spleen, a site of chronic infection, the high levels of depletion in the white pulp at 56 days pi correlated with the high Leishmania parasite burden.