Evidence map›Paper›PMID 35222366›Full record

ArticleFrontiers in immunology2022

Inactivation of AUF1 in Myeloid Cells Protects From Allergic Airway and Tumor Infiltration and Impairs the Adenosine-Induced Polarization of Pro-Angiogenic Macrophages.

Sofia Gargani, Niki Lourou, Christina Arapatzi, Dimitris Tzanos, Marania Saridaki, Esmeralda Dushku, Margarita Chatzimike, Nikolaos D Sidiropoulos, Margarita Andreadou, Vasileios Ntafis and 3 more

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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

13 authors at 2 institutions in 1 country.

Sofia GarganiBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Niki LourouBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Christina ArapatziBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Dimitris TzanosBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Marania SaridakiBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Esmeralda DushkuDepartment of Genetics, Development and Molecular Biology, School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Margarita ChatzimikeBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Nikolaos D SidiropoulosDepartment of Genetics, Development and Molecular Biology, School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Margarita AndreadouBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Vasileios NtafisBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Pantelis HatzisBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Vassiliki KostourouBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Dimitris L KontoyiannisBiomedical Sciences Research Centre "Alexander Fleming", Institute of Fundamental Biomedical Research, Vari, Greece.
Alexander Fleming Biomedical Sciences Research Center · GRAristotle University of Thessaloniki · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The four isoforms of the RNA-binding protein hnRNPD/AUF1 have been proposed to limit the use of inflammatory mRNAs in innate immune cells. Mice engineered to lack AUF1s in all tissues are sensitive to acute inflammatory assaults; however, they also manifest complex degenerations obscuring assessment of AUF1s' roles in innate immune cells. Here, we restricted a debilitating AUF1 mutation to the mouse myeloid lineage and performed disease-oriented phenotypic analyses to assess the requirement of AUF1s in variable contexts of innate immune reactivity. Contrary to the whole-body mutants, the myeloid mutants of AUF1s did not show differences in their susceptibility to cytokine storms occurring during endotoxemia; neither in type-I cell-mediated reactions driving intestinal inflammation by chemical irritants. Instead, they were resistant to allergic airway inflammation and displayed reductions in inflammatory infiltrates and an altered T-helper balance. The

Indexed as

HypersensitivityNeoplasmsAdenosineAnimalsInflammationLungMacrophagesMiceMyeloid CellsRNA, MessengerAdenosineRNA, Messengeranimal modelsinflammationinnate immunitypost-transcriptional regulationRNA-binding proteins

Identifiers

PMID35222366
PMCPMC8873154
OpenAlexW4211101377

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.