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Infection and Immunity, March 2000, p. 1026-1033, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

B Cells Are Essential for Vaccination-Induced Resistance to Virulent Toxoplasma gondii

Peter C. Sayles, George W. Gibson,dagger and Lawrence L. Johnson*

Trudeau Institute, Inc., Saranac Lake, New York 12983

Received 28 June 1999/Returned for modification 5 August 1999/Accepted 29 November 1999

T lymphocytes and gamma interferon (IFN-gamma ) are known mediators of immune resistance to Toxoplasma gondii infection, but whether B cells also play an important role is not clear. We have investigated this issue using B-cell-deficient (µMT) mice. If vaccinated with attenuated T. gondii tachyzoites, µMT mice are susceptible to a challenge intraperitoneal infection with highly virulent tachyzoites that similarly vaccinated B-cell-sufficient mice resist. Susceptibility is evidenced by increased numbers of parasites at the challenge infection site and by extensive mortality. The susceptibility of B-cell-deficient mice does not appear to be caused by deficient T-cell functions or diminished capacity of vaccinated and challenged B-cell-deficient 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. Vaccinated mice lacking Fc receptors or the fifth component of complement resist a challenge infection, suggesting that neither Fc-receptor-dependent phagocytosis of antibody-coated tachyzoites nor antibody-dependent cellular cytotoxicity nor antibody-and-complement-dependent lysis of tachyzoites is a crucial mechanism of resistance. However, Toxoplasma-immune serum effectively inhibits the infection of host cells by tachyzoites in vitro. Together, the results support the hypothesis that B cells are required for vaccination-induced resistance to virulent tachyzoites in order to produce antibodies and that antibodies may function protectively in vivo by blocking infection of host cells by tachyzoites.

* Corresponding author. Mailing address: Trudeau Institute, Inc., P.O. Box 59, Saranac Lake, NY 12983. Phone: (518) 891-3084. Fax: (518) 891-5126. E-mail: ljohnson{at}trudeauinstitute.org.

dagger Present address: Procter and Gamble Pharmaceuticals, Cincinnati, OH 45253-8707.

Infection and Immunity, March 2000, p. 1026-1033, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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