Evidence map›Paper›PMID 25340519›Full record

ArticlePloS one2014

Trypanosoma cruzi evades the protective role of interferon-gamma-signaling in parasite-infected cells.

Philipp Stahl, Volker Ruppert, Ralph T Schwarz, Thomas Meyer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Review
  5. Consensus Enolase ofLife (Basel, Switzerland) · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Frontiers in cellular and infection microbiology · 2020
    Article
  10. The Recombinant Form ofFrontiers in immunology · 2020
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Antimicrobial activity of oleanolic and ursolic acids: an update.Evidence-based complementary and alternative medicine : eCAM · 2015
    Review
  16. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Philipp StahlInstitut für Virologie, AG Parasitologie, Philipps-Universität Marburg, Marburg, Germany.
Volker RuppertKlinik für Kardiologie, Philipps-Universität Marburg, Marburg, Germany.
Ralph T SchwarzInstitut für Virologie, AG Parasitologie, Philipps-Universität Marburg, Marburg, Germany; Unité de Glycobiologie Structurale et Fonctionnelle, UMR CNRS/USTL n° 8576, Université de Lille1 Sciences et Technologies, Villeneuve d'Ascq, France.
Thomas MeyerKlinik für Psychosomatische Medizin und Psychotherapie, Georg-August-Universität Göttingen, Göttingen, Germany.
Philipps University of Marburg · DEUniversité de Lille · FRUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protozoan parasite Trypanosoma cruzi is responsible for the zoonotic Chagas disease, a chronic and systemic infection in humans and warm-blooded animals typically leading to progressive dilated cardiomyopathy and gastrointestinal manifestations. In the present study, we report that the transcription factor STAT1 (signal transducer and activator of transcription 1) reduces the susceptibility of human cells to infection with T. cruzi. Our in vitro data demonstrate that interferon -γ (IFNγ) pre-treatment causes T. cruzi-infected cells to enter an anti-parasitic state through the activation of the transcription factor STAT1. Whereas stimulation of STAT1-expressing cells with IFNγ significantly impaired intracellular replication of parasites, no protective effect of IFNγ was observed in STAT1-deficient U3A cells. The gene encoding indoleamine 2, 3-dioxygenase (ido) was identified as a STAT1-regulated target gene engaged in parasite clearance. Exposure of cells to T. cruzi trypomastigotes in the absence of IFNγ resulted in both sustained tyrosine and serine phosphorylation of STAT1 and its increased DNA binding. Furthermore, we found that in response to T. cruzi the total amount of intracellular STAT1 increased in an infectious dose-dependent manner, both at the mRNA and protein level. While STAT1 activation is a potent strategy of the host in the fight against the invading pathogen, amastigotes replicating intracellularly antagonize this pathway by specifically promoting the dephosphorylation of STAT1 serine 727, thereby partially circumventing its protective effects. These findings point to the crucial role of the IFNγ/STAT1 signal pathway in the evolutionary combat between T. cruzi parasites and their host.

Indexed as

Immune EvasionSignal TransductionAnimalsCell LineChagas DiseaseGene Expression RegulationHumansInterferon-gammaModels, BiologicalParasitesPhosphorylationPhosphoserineSTAT1 Transcription FactorTrypanosoma cruziInterferon-gammaPhosphoserineSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID25340519
PMCPMC4207753
OpenAlexW2021863260

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.