ArticleThe Journal of experimental medicine2016
Toxoplasma gondii TgIST co-opts host chromatin repressors dampening STAT1-dependent gene regulation and IFN-γ-mediated host defenses.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 200 citations in OpenAlex.
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- Comprehensive analysis of Toxoplasma gondii migration routes and tissue dissemination in the host.PLoS neglected tropical diseases · 2025Review
- GRA12 is a common virulence factor across Toxoplasma gondii strains and mouse subspecies.Nature communications · 2025Article
- Immune targeting and host-protective effects of the latent stage of Toxoplasma gondii.Nature microbiology · 2025Article
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- NcROP2 deletion reducesFrontiers in immunology · 2025Article
- Early upregulation of immune suppressors dominates the macrophage response to Toxoplasma gondii.PloS one · 2025Article
- Paracrine rescue of MYR1-deficienteLife · 2024Article
- How Helpful May Be a CRISPR/Cas-Based System for Food Traceability?Foods (Basel, Switzerland) · 2024Review
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- The Toxoplasma oxygen-sensing protein, TgPhyA, is required for resistance to interferon gamma-mediated nutritional immunity in mice.PLoS biology · 2024Article
56 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
An early hallmark of Toxoplasma gondii infection is the rapid control of the parasite population by a potent multifaceted innate immune response that engages resident and homing immune cells along with pro- and counter-inflammatory cytokines. In this context, IFN-γ activates a variety of T. gondii-targeting activities in immune and nonimmune cells but can also contribute to host immune pathology. T. gondii has evolved mechanisms to timely counteract the host IFN-γ defenses by interfering with the transcription of IFN-γ-stimulated genes. We now have identified TgIST (T. gondii inhibitor of STAT1 transcriptional activity) as a critical molecular switch that is secreted by intracellular parasites and traffics to the host cell nucleus where it inhibits STAT1-dependent proinflammatory gene expression. We show that TgIST not only sequesters STAT1 on dedicated loci but also promotes shaping of a nonpermissive chromatin through its capacity to recruit the nucleosome remodeling deacetylase (NuRD) transcriptional repressor. We found that during mice acute infection, TgIST-deficient parasites are rapidly eliminated by the homing Gr1(+) inflammatory monocytes, thus highlighting the protective role of TgIST against IFN-γ-mediated killing. By uncovering TgIST functions, this study brings novel evidence on how T. gondii has devised a molecular weapon of choice to take control over a ubiquitous immune gene expression mechanism in metazoans, as a way to promote long-term parasitism.
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