Background

Visceral leishmaniasis (VL) is a disease caused by systemic infection with protozoa of the genus Leishmania, trans-mitted to mammalian hosts by phlebotomine sandflies. Human VL is characterized by fever, hepatosplenomegaly, anemia, leukopenia, and severe weight loss and is fatal if not treated. VL is associated with a marked impairment of leishmania-specific Th1 response, as evaluated by in vitro leishmania antigen stimulation of peripheral blood mononuclear cells (PBMC) [1]. However, high levels of proinflammatory cytokines, including IFN-γ, have been detected in serum and bone marrow of VL patients [2-4]. IL-12 and IFN-γ have been associated with a protective immunity in individuals living in an endemic area [5]. These cytokines activate macrophages to release several microbicidal agents to kill the parasites [6]. High amounts of IL-10 are also detected in sera and bone marrow of V