Figure 4

A schematic view of the immune responses in BALB/c mice livers after experimental infection with L. infantum. After intravenous inoculation, the parasites enter the liver and invade macrophages and DCs. (A) During the hepatic acute phase (up to two weeks pi), Leishmania amastigotes multiply in the absence of both IL-12 production and activated T-cells. Consequently, the number of parasites in the liver reaches a peak. (B) Two weeks pi, Leishmania-specific T lymphocytes migrate to the liver from the spleen and the acquired hepatic immune response is initiated. The interaction of Leishmania-specific T cells with infected KCs and DCs provides the proinflammatory (Th1) environment required for efficient granuloma formation, resulting in the resolution of hepatic infection. (C) The kinetics of parasite burden and different stages of granuloma maturation in the liver after L. infantum infection. Infected KCs with no granulomatous reaction and immature granulomas were observed in high numbers at 14 days pi but these initial stages of granuloma formation decreased in number during the course of infection, developing mature and sterile granulomas. Significantly, by 56 days pi, the number of sterile granulomas, in which the amastigotes were killed, increased and consequently, the Leishmania parasite burden decreased. Finally, the infection in the liver of BALB/c mice was resolved.