Decreased resistance of B cell-deficient mice to infection with Toxoplasmagondii despite unimpaired expression of IFN-gamma, TNF-alpha, and inducible nitric oxide synthase

The role of B cells in resistance against Toxoplasma gondii was studied usi ng B cell-deficient (mu MT) mice. Following peroral infection with 10 cysts of the ME49 strain, all mu MT mice survived the acute stage of the infecti on but died between 3 and 4 wk after infection. In contrast, all control mi ce were alive at 8 wk after infection; At the stage during which mu MT anim als succumbed to the infection, parasite replication and pathology were mos t evident in their brains; small numbers of tachyzoites were also detectabl e in their lungs. Significantly greater numbers of T, gondii cysts and area s of inflammation associated with tachyzoites were observed in brains of mu MT than in control mice, Large areas of necrosis associated with numerous tachyzoites were observed only in brains of mu MT mice, Anti-T, gondii IgG Abs were detected only in sera of control mice, whereas similar levels of I FN-gamma were detected in sera of both strains of mice. Amounts of mRNA for IFN-gamma, IL010, and inducible NO synthase in the brain did not differ be tween infected mu MT and control mice. Expression of mRNA for TNF-alpha was increased in brains of mu MT mice. Administration of polyclonal rabbit ant i-T. gondii IgG Ab prevented early mortality and pathology associated with tachyzoites in the brain in the infected mu MT 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.