A role has been proposed for inflammatory mediators such as gamma interferon (IFN-γ) and reactive oxygen intermediates in the control of the blood stages of Plasmodium organisms. It was previously shown that IFN-γ 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-γ, suggesting that susceptibilityy is not due to a defect in IFN-γ production. Administration of IFN-γ to intact C57BL/6 mice slightly decreased and partially delayed parasitemia, whereas in vivo depletion of IFN-γ through injection of a 'cocktail' of monoclonal antibodies agains IFN-γ 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-γ production in vivo and whether exogenous IFN-γ can replace the protective function of the CD4+ T cells. Mice depleted of CD4+ T cells were unable to produce IFN-γ, but factors in addition to IFN-γ may be important in parasite clearance.
CITATION STYLE
Meding, S. J., Cheng, S. C., Simon-Haarhaus, B., & Langhorne, J. (1990). Role of gamma interferon during infection with Plasmodium chabaudi chabaudi. Infection and Immunity, 58(11), 3671–3678. https://doi.org/10.1128/iai.58.11.3671-3678.1990
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