Evidence map›Paper›PMID 35812461›Full record

ArticleFrontiers in immunology2022

Fra-2 Is a Dominant Negative Regulator of Natural Killer Cell Development.

Diana Schnoegl, Mathias Hochgerner, Dagmar Gotthardt, Leigh M Marsh

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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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 1 country.

Diana SchnoeglLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Mathias HochgernerLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Dagmar GotthardtInstitute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria.
Leigh M MarshLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Ludwig Boltzmann Institute for Lung Vascular Research · ATMedical University of Graz · ATUniversity of Veterinary Medicine Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK) cells play an important role in recognizing and killing pathogen-infected or malignant cells. Changes in their numbers or activation can contribute to several diseases and pathologies including systemic sclerosis (SSc), an autoimmune disease characterized by inflammation and tissue remodeling. In these patients, increased expression of the AP-1 transcription factor, Fra-2 was reported. In mice ectopic overexpression of Fra-2 (TG) leads to SSc with strong pulmonary fibrosis, pulmonary hypertension, and inflammation. Analysis of the underlying immune cell profile in the lungs of young TG mice, which do not yet show any signs of lung disease, revealed increased numbers of eosinophils and T cells but strongly reduced NK numbers. Therefore, we aimed to identify the cause of the absence of NK cells in the lungs of these mice and to determine the potential role of Fra-2 in NK development. Examination of inflammatory cell distribution in TG mice revealed similar NK deficiencies in the spleen, blood, and bone marrow. Deeper analysis of the WT and TG bone marrow revealed a potential NK cell developmental defect beginning at the preNKP stage. To determine whether this defect was cell-intrinsic or extrinsic, mixed bone marrow chimera and

Indexed as

Scleroderma, SystemicTranscription Factor AP-1AnimalsFos-Related Antigen-2InflammationKiller Cells, NaturalMiceFosl2 protein, mouseFos-Related Antigen-2Transcription Factor AP-1activator protein 1AP-1differentiationFra-2innate immunityNatural killer (NK) cell

Identifiers

PMID35812461
PMCPMC9257261
OpenAlexW4283364819

What OpenQuestion holds

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LicenceCC BY
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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.