Emergence of NK1.1+ cells as effectors of IFN-gamma dependent immunity to Toxoplasma gondii in MHC class I-deficient mice.

摘要: CD8+ T lymphocytes have been reported to play a major role in the protective immune response against acute infection with Toxoplasma gondii. In order further assess of cells resistance this protozoan we examined ability beta 2m-deficient mice, which fail express MHC class I molecules and peripheral lymphocytes, survive tachyzoite challenge following vaccination an attenuated parasite mutant. Surprisingly, mice induced strong lethal challenge, > 50% surviving beyond 3 months. Vaccinated but not control heterozygotes, showed five- six-fold expansion spleen cell number approximately 40% splenocytes were found NK markers NK1.1 asialo GM1. Spleen from vaccinated animals failed kill either infected host or target YAC-1. However, high levels IFN-gamma secreted when cultured vitro soluble T. gondii lysate, was abolished by NK1.1+ CD4+ lymphocyte depletion, implicating population as source IFN-gamma. More importantly, vaccine-induced immunity completely abrogated vivo administration antibody NK1.1, GM1, Together, data suggest that I-deficient gondii, absence effector is compensated for emergence GM1+ lack cytolytic activity, action these attributable production. The induction novel may provide approach controlling opportunistic infections immunocompromised hosts.