Decreased resistance of B cell-deficient mice to infection with Toxoplasma gondii despite unimpaired expression of IFN-γ, TNF-α, and inducible nitric oxide synthase

The role of B cells in resistance against Toxoplasma gondii was studied using B cell-deficient (μMT) mice. Following peroral infection with 10 cysts of the ME49 strain, all μMT mice survived the acute stage of the infection but died between 3 and 4 wk after infection. In contrast, all control mice were alive at 8 wk after infection. At the stage during which μMT animals succumbed to the infection, parasite replication and pathology were most evident in their brains; small numbers of tachyzoites were also detectable in their lungs. Significantly greater numbers of T. gondii cysts and areas of inflammation associated with tachyzoites were observed in brains of μMT than in control mice. Large areas of necrosis associated with numerous tachyzoites were observed only in brains of μMT mice. Anti. T. gondii IgG Abs were detected only in sera of control mice, whereas similar levels of IFN-γ, were detected in sera of both strains of mice. Amounts of mRNA for IFN-γ IL-10, and inducible NO synthase in the brain did not differ between infected μMT and control mice. Expression of mRNA for TNF-α was increased in brains of μMT mice. Administration of polyclonal rabbit anti-T. gondii IgG Ab prevented early mortality and pathology associated with tachyzoites in the brain in the infected μMT mice. These results indicate that B cells play an important role, most likely through their production of specific Abs, in resistance to persistent active (tachyzoite) infection with T. gondii in mice, especially in the brain and lung.