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Cited by 179

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IFN-γ Overproduction and High Level Apoptosis Are Associated with High but Not Low Virulence Toxoplasma gondii Infection

Open access
Gavrilescu, L Cristina, Denkers, Eric Y·2001·The Journal of Immunology

Abstract

Toxoplasma gondii is an opportunistic intracellular parasite which induces a highly strong type 1 cytokine response. The present study focuses on defining the factors influencing the outcome of infection with tachyzoites of the type I, highly lethal RH strain, relative to the type II, low virulence strain ME49. Infection with the RH strain led to widespread parasite dissemination and rapid death of mice; in contrast, mice survived low virulence strain ME49 infection, and tachyzoite dissemination was much less extensive. Furthermore, massive apoptosis and disintegration of the splenic architecture was characteristic of RH, but not ME49, infection. In addition, hyperinduction of IFN-γ and lack of NO production were found during RH, in contrast to ME49 infection. These data demonstrate that Toxoplasma strain characteristics exert a profound effect on the host immune response and that the latter itself is a crucial determinant in parasite virulence.

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Crossref · 10.4049/jimmunol.167.2.902

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Metadata

Authors
Gavrilescu, L. C., & Denkers, E. Y.
Venue
The Journal of Immunology
Published
2001-07
Volume
167
Issue
2
Pages
902-909
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W2138814634
Cited by
179
References
1
FWCI
7.21
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: IFN-γ Overproduction and High Level Apoptosis Are Associated with High but Not Low Virulence Toxoplasma gondii Infection. https://app.cochat.ai/papers/10.4049/jimmunol.167.2.902
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Gavrilescu, L. C., & Denkers, E. Y. (2001). IFN-γ Overproduction and High Level Apoptosis Are Associated with High but Not Low Virulence Toxoplasma gondii Infection. The Journal of Immunology. https://doi.org/10.4049/jimmunol.167.2.902

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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