CD8 + T lymphocytes have been reported to play a major role in the protective immune response against acute infection with Toxoplasma gondii. In order to further assess the role of CD8 + cells in resistance against this protozoan we examined the ability of B2m-deficient mice, which fail to express MHC class I molecules and peripheral CD8 + lymphocytes, to survive tachyzoite challenge following vaccination with an attenuated parasite mutant. Surprisingly, vaccination of B2m-deficient mice induced strong resistance to lethal challenge, with>50 % surviving beyond 3 months. Vaccinated ~2m-deficient mice, but not control heterozygotes, showed a five- to sixfold expansion in spleen cell number and "~40 % of the splenocytes were found to express the NK markers NKI.1 and asialo GMI. Spleen cells from the vaccinated/~2m-deficient animals failed to kill either infected host cells or the NK target YAC-1. However, high levels of IFN-3 ~ were secreted when the cells were cultured in vitro with soluble T. gondii lysate, and this response was abolished by NKI.1 § but not CD4 + and CD8 § lymphocyte depletion, implicating the NKI.1 + population as the major source of IFN- % More importantly, vaccine-induced immunity in fl2m-deficient mice was completely abrogated by in vivo administration of antibody to NKI.1, asialo GM1, or IFN- % Together, the data suggest that in class I-deficient mice vaccinated agains
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