Experimental Leishmania major infection in mice:: role of IL-10

L. major infection of mice induces polarized Th1 and Th2 responses that are correlated with healing of the infection (Th1) or a fatal disease (Th2). The Th subset specific cytokines, IFN gamma and IL-4, themselves were shown to be important factors for the differentiation into the;Th1 and Th2 pathways during infection. We studied the role of the Th2 cytokine IL-10 during leishmania infection: removal of endogenous IL-10 by anti-IL-10 treatment did not alter the Th2 cytokine pattern in non-healer mice nor did it modulate DTH reactivity, IgE production or fatal disease progression, bur partially blocked the IFN gamma inhibiting effect of rIL-4 in healer mice. During chronic infection similar amounts of IL-10 were produced in both healer and non-healer mice. However, at early time-points during infection IL-IO production was significantly higher in the non-healer;Th2 responder animals. IL-IO production in vitro caused significant inhibition of in vitro IFN gamma production. In conclusion IL-IO, unlike IL-4 and IFN gamma does not seem to play a readily detectable role in the Th subset differentiation during L. major infection. However, the high production of IL-IO early during infection in non-healer mice and inhibition of leishmania-specific IFN gamma production may contribute to drive the immune response cowards a: Th2 response.