Role of gamma interferon during infection with Plasmodium chabaudi chabaudi

Abstract

A role has been proposed for inflammatory mediators such as gamma interferon (IFN-gamma) and reactive oxygen intermediates in the control of the blood stages of Plasmodium organisms. It was previously shown that IFN-gamma can be detected in the plasma of mice with a primary infection by Plasmodium chabaudi chabaudi (AS). We found that susceptible and other resistant mouse strains produced IFN-gamma, suggesting that susceptibility is not due to a defect in IFN-gamma production. Administration of IFN-gamma to intact C57BL/6 mice slightly decreased and partially delayed parasitemia, whereas in vivo depletion of IFN-gamma through injection of a "cocktail" of monoclonal antibodies against IFN-gamma exacerbated infection. Since CD4+ T cells are essential for the development of a protective immune response to P. chabaudi chabaudi, we tested whether CD4+ T cells are responsible for IFN-gamma production in vivo and whether exogenous IFN-gamma can replace the protective function of the CD4+ T cells. Mice depleted of CD4+ T cells were unable to produce IFN-gamma, but factors in addition to IFN-gamma may be important in parasite clearance.