ArticlePloS one2013
Toxoplasma gondii triggers phosphorylation and nuclear translocation of dendritic cell STAT1 while simultaneously blocking IFNγ-induced STAT1 transcriptional activity.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Key Regulators of Parasite Biology Viewed Through a Post-Translational Modification Repertoire.Proteomics · 2025Review
- Transcriptomics ofMicroorganisms · 2024Article
- IFNs in host defence and parasite immune evasion duringFrontiers in immunology · 2024Review
- Overview of Apoptosis, Autophagy, and Inflammatory Processes inPathogens (Basel, Switzerland) · 2023Review
- Gene Regulation Analysis Reveals Perturbations of Autism Spectrum Disorder during Neural System Development.Genes · 2021Article
- Seizing control: How dense granule effector proteins enable Toxoplasma to take charge.Molecular microbiology · 2021Review
- Modulation Effects ofVaccines · 2020Article
- Cell type- and species-specific host responses to Toxoplasma gondii and its near relatives.International journal for parasitology · 2020Review
- ROP18-Mediated Transcriptional Reprogramming of HEK293T Cell Reveals New Roles of ROP18 in the Interplay BetweenFrontiers in cellular and infection microbiology · 2020Article
- Epigenetic Control of IFN-γ Host Responses During Infection WithFrontiers in immunology · 2020Article
- Transcriptome analysis of the effect of C-C chemokine receptor 5 deficiency on cell response to Toxoplasma gondii in brain cells.BMC genomics · 2019Article
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- Toxoplasma gondii ROP17 inhibits the innate immune response of HEK293T cells to promote its survival.Parasitology research · 2019Article
- Downregulation of the Central Noradrenergic System byInfection and immunity · 2019Article
- Regulation of NF-κB- and STAT1-mediated plasmacytoid dendritic cell functions by A20.PloS one · 2019Article
- Rhoptry and Dense Granule Secreted Effectors Regulate CD8Frontiers in immunology · 2019Article
- Toxoplasma gondii Manipulates Expression of Host Long Noncoding RNA during Intracellular Infection.Scientific reports · 2018Article
- Chloroquine-treated dendritic cells require STAT1 signaling for their tolerogenic activity.European journal of immunology · 2018Article
- Integrative Approaches to Understand the Mastery in Manipulation of Host Cytokine Networks by Protozoan Parasites with Emphasis onFrontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The protozoan Toxoplasma gondii actively modulates cytokine-induced JAK/STAT signaling pathways to facilitate survival within the host, including blocking IFNγ-mediated STAT1-dependent proinflammatory gene expression. We sought to further characterize inhibition of STAT1 signaling in infected murine dendritic cells (DC) because this cell type has not previously been examined, yet is known to serve as an early target of in vivo infection. Unexpectedly, we discovered that T. gondii infection alone induced sustained STAT1 phosphorylation and nuclear translocation in DC in a parasite strain-independent manner. Maintenance of STAT1 phosphorylation required active invasion but intracellular parasite replication was dispensable. The parasite rhoptry protein ROP16, recently shown to mediate STAT3 and STAT6 phosphorylation, was not required for STAT1 phosphorylation. In combination with IFNγ, T. gondii induced synergistic STAT1 phosphorylation and binding of aberrant STAT1-containing complexes to IFNγ consensus sequence oligonucleotides. Despite these findings, parasite infection blocked STAT1 binding to the native promoters of the IFNγ-inducible genes Irf-1 and Lrg47, along with subsequent gene expression. These results reinforce the importance of parasite-mediated blockade of IFNγ responses in dendritic cells, while simultaneously showing that T. gondii alone induces STAT1 phosphorylation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.