Related Experiment Video

Updated: May 13, 2026

Forward Genetics Screens Using Macrophages to Identify Toxoplasma gondii Genes Important for Resistance to IFN-γ-Dependent Cell Autonomous Immunity
11:21

Forward Genetics Screens Using Macrophages to Identify Toxoplasma gondii Genes Important for Resistance to IFN-γ-Dependent Cell Autonomous Immunity

Published on: March 12, 2015

Toxoplasma gondii triggers phosphorylation and nuclear translocation of dendritic cell STAT1 while simultaneously

Anne G Schneider1, Delbert S Abi Abdallah, Barbara A Butcher

  • 1Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York, United States of America.

Plos One
|March 26, 2013
PubMed

Insights

Toxoplasma gondii infection triggers STAT1 phosphorylation in dendritic cells, despite blocking downstream gene expression. This parasite strategy aids survival by manipulating host immune signaling pathways.

Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • Toxoplasma gondii manipulates host JAK/STAT signaling for survival.
  • IFNγ-induced STAT1 signaling is crucial for controlling protozoan infections.
  • Dendritic cells are early targets of T. gondii infection.

Purpose of the Study:

  • To investigate STAT1 signaling inhibition by T. gondii in murine dendritic cells.
  • To characterize the parasite's mechanism of modulating host immune responses.

Main Methods:

  • Murine dendritic cells were infected with T. gondii.
  • STAT1 phosphorylation and nuclear translocation were assessed.
  • IFNγ-inducible gene expression and promoter binding were analyzed.

Main Results:

  • T. gondii infection alone induced sustained STAT1 phosphorylation and nuclear translocation in dendritic cells.
  • Active invasion was necessary, but parasite replication was not, for STAT1 phosphorylation.
  • T. gondii blocked STAT1 binding to key IFNγ-inducible gene promoters, inhibiting their expression.

Conclusions:

  • T. gondii actively induces STAT1 phosphorylation in dendritic cells independently of IFNγ.
  • The parasite effectively blocks IFNγ-mediated inflammatory gene expression in dendritic cells.
  • This highlights a novel immune evasion mechanism by T. gondii.

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