Evidence map›Paper›PMID 34322123›Full record

ArticleFrontiers in immunology2021

Myeloid-Derived Suppressor Cells Dampen Airway Inflammation Through Prostaglandin E2 Receptor 4.

Chiel van Geffen, Astrid Deißler, Sandra Beer-Hammer, Bernd Nürnberg, Rupert Handgretinger, Harald Renz, Dominik Hartl, Saeed Kolahian

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Characterizing the Emergence of Myeloid-Derived Suppressor Cell Subsets in a Murine Model of Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. Observational
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  10. 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

8 authors at 3 institutions in 2 countries.

Chiel van GeffenDepartment of Experimental and Clinical Pharmacology and Pharmacogenomics, University Hospital Tübingen, Tübingen, Germany.
Astrid DeißlerDepartment of Experimental and Clinical Pharmacology and Pharmacogenomics, University Hospital Tübingen, Tübingen, Germany.
Sandra Beer-HammerDepartment of Pharmacology, Experimental Therapy & Toxicology and Interfaculty Center of Pharmacogenomics & Drug Research (IZePhA), University Hospitals and Clinics, Eberhard Karls University Tübingen, Tübingen, Germany.
Bernd NürnbergDepartment of Pharmacology, Experimental Therapy & Toxicology and Interfaculty Center of Pharmacogenomics & Drug Research (IZePhA), University Hospitals and Clinics, Eberhard Karls University Tübingen, Tübingen, Germany.
Rupert HandgretingerChildren's University Hospital, Eberhard Karls University of Tübingen, Tübingen, Germany.
Harald RenzInstitute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University of Marburg, Marburg, Germany.
Dominik HartlDepartment of Pediatrics I, Eberhard Karls University of Tübingen, Tübingen, Germany.
Saeed KolahianDepartment of Experimental and Clinical Pharmacology and Pharmacogenomics, University Hospital Tübingen, Tübingen, Germany.
Universities of Giessen and Marburg Lung Center · DEUniversity of Tübingen · DEUniversity Children's Hospital Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence suggests a mechanistic role for myeloid-derived suppressor cells (MDSCs) in lung diseases like asthma. Previously, we showed that adoptive transfer of MDSCs dampens lung inflammation in murine models of asthma through cyclooxygenase-2 and arginase-1 pathways. Here, we further dissected this mechanism by studying the role and therapeutic relevance of the downstream mediator prostaglandin E2 receptor 4 (EP4) in a murine model of asthma. We adoptively transferred MDSCs generated using an EP4 agonist in a murine model of asthma and studied the consequences on airway inflammation. Furthermore, pegylated human arginase-1 was used to model MDSC effector activities. We demonstrate that the selective EP4 agonist L-902,688 increased the number and suppressive activity of MDSCs through arginase-1 and nitric oxide synthase-2. These results showed that adoptive transfer of EP4-primed MDSCs, EP4 agonism alone or arginase-1 administration ameliorated lung inflammatory responses and histopathological changes in asthmatic mice. Collectively, our results provide evidence that MDSCs dampen airway inflammation in murine asthma through a mechanism involving EP4.

Indexed as

Adoptive TransferAnimalsAntigens, DermatophagoidesArginaseArthropod ProteinsAsthmaCells, CulturedCytokinesDinoprostoneDisease Models, AnimalFemaleLungMiceMice, Inbred BALB CMyeloid-Derived Suppressor CellsNitric Oxide Synthase Type IIAntigens, DermatophagoidesARG1 protein, humanArg1 protein, mouseArginaseArthropod ProteinsCytokinesDinoprostoneL-902688Nitric Oxide Synthase Type IINos2 protein, mousePtger2 protein, mousePtger4 protein, mousePyrrolidinonesReceptors, Prostaglandin E, EP2 SubtypeReceptors, Prostaglandin E, EP4 SubtypeTetrazolesairway inflammationarginase-1asthmaE-prostanoid receptorsmyeloid-derived suppressor cellsprostaglandin E2

Identifiers

PMID34322123
PMCPMC8311661
OpenAlexW3177604832

What OpenQuestion holds

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Registered trials

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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.