B cells are essential for vaccination-induced resistance to virulent Toxoplasma gondii

T lymphocytes and gamma interferon (IFN-gamma) are known mediators of immun e resistance to Toxoplasma gondii infection, but whether B cells also play an important role is not clear. We have investigated this issue using B-cel l-deficient (mu MT) mice. If vaccinated with attenuated T. gondii tachyzoit es, mu MT mice are susceptible to a challenge intraperitoneal infection wit h highly virulent tachyzoites that similarly vaccinated B-cell-sufficient m ice resist. Susceptibility is evidenced by increased numbers of parasites a t the challenge infection site and by extensive mortality. The susceptibili ty of B-cell-deficient mice does not appear to be caused by deficient T-cel l functions or diminished capacity of vaccinated and challenged B-cell-defi cient mice to produce IFN-gamma. Administration of Toxoplasma-immune serum, but not nonimmune serum, to vaccinated B-cell-deficient mice significantly prolongs their survival after challenge with virulent tachyzoites. Vaccina ted mice lacking Fe receptors or the fifth component of complement resist a challenge infection, suggesting that neither Fc-receptor-dependent phagocy tosis of antibody-coated tachyzoites nor antibody-dependent cellular cytoto xicity nor antibody-and-complement-dependent lysis of tachyzoites is a cruc ial mechanism of resistance. However, Toxoplasma-immune serum effectively i nhibits the infection of host cells by tachyzoites in vitro. Together, the results support the hypothesis that B cells are required for vaccination-in duced resistance to virulent tachyzoites in order to produce antibodies and that antibodies may function protectively in vivo by blacking infection of host cells by tachyzoites.