Evidence map›Paper›PMID 29780382›Full record

ArticleFrontiers in immunology2018

Extracellular Purine Metabolism Is the Switchboard of Immunosuppressive Macrophages and a Novel Target to Treat Diseases With Macrophage Imbalances.

Anna Ohradanova-Repic, Christian Machacek, Celine Charvet, Franck Lager, Delphine Le Roux, René Platzer, Vladimir Leksa, Goran Mitulovic, Thomas R Burkard, Gerhard J Zlabinger and 11 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  10. ProbioticInternational journal of molecular sciences · 2024
    Article
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  13. iScience · 2023
    Article
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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

21 authors at 9 institutions in 6 countries.

Anna Ohradanova-RepicMolecular Immunology Unit, Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Christian MachacekMolecular Immunology Unit, Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Celine CharvetInstitut National de la Santé et de la Recherche Médicale, INSERM U1016, Institut Cochin, Paris, France.
Franck LagerInstitut National de la Santé et de la Recherche Médicale, INSERM U1016, Institut Cochin, Paris, France.
Delphine Le RouxInstitut National de la Santé et de la Recherche Médicale, INSERM U1016, Institut Cochin, Paris, France.
René PlatzerMolecular Immunology Unit, Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Vladimir LeksaMolecular Immunology Unit, Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Goran MitulovicClinical Department of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria.
Thomas R BurkardBioinformatics Department of the Research Institute of Molecular Pathology and the Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
Gerhard J ZlabingerInstitute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Michael B FischerDepartment of Transfusion Medicine, Medical University of Vienna, Vienna, Austria.
Vincent FeuilletInstitut National de la Santé et de la Recherche Médicale, INSERM U1016, Institut Cochin, Paris, France.
Gilles RenaultInstitut National de la Santé et de la Recherche Médicale, INSERM U1016, Institut Cochin, Paris, France.
Stephan BlümlDivision of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Miroslav BenkoEXBIO Praha, Vestec, Czechia.
Miloslav SuchanekEXBIO Praha, Vestec, Czechia.
Johannes B HuppaMolecular Immunology Unit, Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Takami MatsuyamaThe Center for Advanced Biomedical Sciences and Swine Research, Kagoshima University, Kagoshima, Japan.
Artur Cavaco-PauloCentre of Biological Engineering, University of Minho, Campus of Gualtar, Braga, Portugal.
Georges BismuthInstitut National de la Santé et de la Recherche Médicale, INSERM U1016, Institut Cochin, Paris, France.
Hannes StockingerMolecular Immunology Unit, Institute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATInserm · FRExbio (Czechia) · CZInstitut Cochin · FRDélégation Paris 5 · FRInstitute of Molecular Biology of the Slovak Academy of Sciences · SKInstitute of Molecular Biotechnology · ATKagoshima University · JPUniversity of Minho · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

If misregulated, macrophage (Mϕ)-T cell interactions can drive chronic inflammation thereby causing diseases, such as rheumatoid arthritis (RA). We report that in a proinflammatory environment, granulocyte-Mϕ (GM-CSF)- and Mϕ colony-stimulating factor (M-CSF)-dependent Mϕs have dichotomous effects on T cell activity. While GM-CSF-dependent Mϕs show a highly stimulatory activity typical for M1 Mϕs, M-CSF-dependent Mϕs, marked by folate receptor β (FRβ), adopt an immunosuppressive M2 phenotype. We find the latter to be caused by the purinergic pathway that directs release of extracellular ATP and its conversion to immunosuppressive adenosine by co-expressed CD39 and CD73. Since we observed a misbalance between immunosuppressive and immunostimulatory Mϕs in human and murine arthritic joints, we devised a new strategy for RA treatment based on targeted delivery of a novel methotrexate (MTX) formulation to the immunosuppressive FRβ

Indexed as

Cell DifferentiationAdenosineAnimalsArthritis, RheumatoidCell ProliferationDisease Models, AnimalGranulocyte-Macrophage Colony-Stimulating FactorHumansImmunosuppressive AgentsInflammationMacrophage Colony-Stimulating FactorMacrophagesMaleMethotrexateMiceMonocytesAdenosineGranulocyte-Macrophage Colony-Stimulating FactorImmunosuppressive AgentsMacrophage Colony-Stimulating FactorMethotrexatePurinesadenosinechronic inflammationmacrophage polarizationmacrophage-T cell interactionmethotrexatepurine metabolismrheumatoid arthritis

Identifiers

PMID29780382
PMCPMC5946032
OpenAlexW2800260093

What OpenQuestion holds

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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.