Evidence map›Paper›PMID 22719255›Full record

ArticlePLoS pathogens2012

Conditional Stat1 ablation reveals the importance of interferon signaling for immunity to Listeria monocytogenes infection.

Elisabeth Kernbauer, Verena Maier, Dagmar Stoiber, Birgit Strobl, Christine Schneckenleithner, Veronika Sexl, Ursula Reichart, Boris Reizis, Ulrich Kalinke, Amanda Jamieson and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Curdlan LimitsFrontiers in microbiology · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

12 authors at 6 institutions in 3 countries.

Elisabeth KernbauerMax F. Perutz Laboratories, University of Vienna, Vienna, Austria.
Verena Maier
Dagmar Stoiber
Birgit Strobl
Christine Schneckenleithner
Veronika Sexl
Ursula Reichart
Boris Reizis
Ulrich Kalinke
Amanda Jamieson
Mathias Müller
Thomas Decker
University of Veterinary Medicine Vienna · ATMax Perutz Labs · ATUniversity of Vienna · ATCenter for Experimental and Clinical Infection Research · DEColumbia University Irving Medical Center · USMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducer and activator of transcription 1 (Stat1) is a key player in responses to interferons (IFN). Mutations of Stat1 cause severe immune deficiencies in humans and mice. Here we investigate the importance of Stat1 signaling for the innate and secondary immune response to the intracellular bacterial pathogen Listeria monocytogenes (Lm). Cell type-restricted ablation of the Stat1 gene in naïve animals revealed unique roles in three cell types: macrophage Stat1 signaling protected against lethal Lm infection, whereas Stat1 ablation in dendritic cells (DC) did not affect survival. T lymphocyte Stat1 reduced survival. Type I IFN (IFN-I) signaling in T lymphocytes reportedly weakens innate resistance to Lm. Surprisingly, the effect of Stat1 signaling was much more pronounced, indicating a contribution of Stat1 to pathways other than the IFN-I pathway. In stark contrast, Stat1 activity in both DC and T cells contributed positively to secondary immune responses against Lm in immunized animals, while macrophage Stat1 was dispensable. Our findings provide the first genetic evidence that Stat1 signaling in different cell types produces antagonistic effects on innate protection against Lm that are obscured in mice with complete Stat1 deficiency. They further demonstrate a drastic change in the cell type-dependent Stat1 requirement for memory responses to Lm infection.

Indexed as

Adoptive TransferAnimalsDendritic CellsFlow CytometryImmunity, InnateImmunologic MemoryInterferon Type IListeria monocytogenesListeriosisMacrophagesMiceMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionSignal TransductionSTAT1 Transcription FactorInterferon Type IStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID22719255
PMCPMC3375314
OpenAlexW2070026001

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.