Affiliation:
1. Department of Immunology and Infectious Diseases, Research Institute, Palo Alto Medical Foundation, Palo Alto, California 94301, and Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305
Abstract
ABSTRACT
We examined the mechanism of resistance against reactivation of infection with
Toxoplasma gondii
in the brain. BALB/c-background gamma interferon (IFN-γ)-knockout (IFN-γ
−/−
) and control mice were infected and treated with sulfadiazine beginning 4 days after infection for 3 weeks. After discontinuation of treatment, IFN-γ
−/−
mice succumbed to toxoplasmic encephalitis (TE) and died, whereas control animals did not develop TE and survived. Adoptive transfer of immune spleen cells from infected control mice did not prevent development of TE or mortality in the IFN-γ
−/−
mice. To examine whether the failure of the cell transfer to protect against TE is unique to IFN-γ
−/−
mice, athymic nude and SCID mice that lack T cells were infected and injected with the immune spleen or T cells in the same manner as IFN-γ
−/−
mice. Whereas control nude and SCID mice that had not received the immune cells developed severe TE and died after discontinuation of sulfadiazine, those that had received the cells did not develop TE and survived. Before cell transfer, IFN-γ mRNA was detected in brains of infected nude and SCID but not in brains of IFN-γ
−/−
mice. IFN-γ mRNA was also detected in brains of infected SCID mice depleted of NK cells by treatment with anti-asialo GM1 antibody, and such animals did not develop TE after receiving immune T cells. Thus, IFN-γ production by non-T cells, in addition to T cells, is required for prevention of reactivation of
T. gondii
infection in the brain. The IFN-γ-producing non-T cells do not appear to be NK cells.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
68 articles.
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