Protective-immunity to erythrocytic Plasmodium chabaudi AS infection involves IFN gamma-mediated responses and a cellular infiltrate to the liver

IFN gamma receptor (IFN gammaR) deficient mice and IL-4 deficient mice were infected with blood-stage Plasmodium chabaudi AS in order to analyse the r ole of Th1 (IFN gamma) and Th2 (IL-4)-associated cytokines in the developme nt of protective immunity to the parasite. A high mortality rate and failur e to reduce the primary parasitaemia to subpatent levels was observed in th e IFN gammaR deficient mice. IL-4 deficient mice controlled a primary P. ch abaudi AS infection in a similar manner to control mice and no mortality wa s observed. IFN gammaR deficient mice had a reduction in parasite-specific IgG and a significantly increased level of total IgE compared to control mi ce. There was no reduction in the level of parasite-specific IgG in IL-4 de ficient mice. Cytological analysis of the cells present in the spleen and l iver during the primary parasitaemia revealed a reduction;in the numbers of lymphocytes, monocytes and polymorphonuclear (PMN) cells in the liver at t he peak of parasitaemia in both IFN gammaR deficient mice and IL-4 deficien t mice compared to control mice. Adoptive transfer studies demonstrated tha t cells isolated from the liver at day 11 post-infection could confer some protective immunity to P. chabaudi AS infection.