Evidence map›Paper›PMID 29742141›Full record

ArticlePloS one2018

CD39 is upregulated during activation of mouse and human T cells and attenuates the immune response to Listeria monocytogenes.

Friederike Raczkowski, Anne Rissiek, Isabell Ricklefs, Kirsten Heiss, Valéa Schumacher, Kira Wundenberg, Friedrich Haag, Friedrich Koch-Nolte, Eva Tolosa, Hans-Willi Mittrücker

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  4. Therapeutic potential of CD73Histology and histopathology · 2025
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  11. Low Pretreatment CD4International journal of molecular sciences · 2023
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  14. T-Cell Receptor Repertoire Sequencing in the Era of Cancer Immunotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. 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

10 authors at 1 institution in 1 country.

Friederike RaczkowskiInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anne RissiekInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Isabell RicklefsInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Kirsten HeissInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Valéa SchumacherInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Kira WundenbergInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Friedrich HaagInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Friedrich Koch-NolteInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Eva TolosaInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hans-Willi MittrückerInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0001-6166-4191
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ectoenzymes CD39 and CD73 degrade extracellular ATP to adenosine. ATP is released by stressed or damaged cells and provides pro-inflammatory signals to immune cells through P2 receptors. Adenosine, on the other hand, suppresses immune cells by stimulating P1 receptors. Thus, CD39 and CD73 can shape the quality of immune responses. Here we demonstrate that upregulation of CD39 is a consistent feature of activated conventional CD4+ and CD8+ T cells. Following stimulation in vitro, CD4+ and CD8+ T cells from human blood gained surface expression of CD39 but displayed only low levels of CD73. Activated human T cells from inflamed joints largely presented with a CD39+CD73- phenotype. In line, in spleens of mice with acute Listeria monocytogenes, listeria-specific CD4+ and CD8+ T cells acquired a CD39+CD73- phenotype. To test the function of CD39 in control of bacterial infection, CD39-deficient (CD39-/-) mice were infected with L. monocytogenes. CD39-/- mice showed better initial control of L. monocytogenes, which was associated with enhanced production of inflammatory cytokines. In the late stage of infection, CD39-/- mice accumulated more listeria-specific CD8+ T cells in the spleen than wildtype animals suggesting that CD39 attenuates the CD8+ T-cell response to infection. In conclusion, our results demonstrate that CD39 is upregulated on conventional CD4+ and CD8+ T cells at sites of acute infection and inflammation, and that CD39 dampens responses to bacterial infection.

Indexed as

AnimalsAntigens, CDApyraseCD8-Positive T-LymphocytesFlow CytometryGene Expression RegulationHumansImmunity, InnateInfectionsInflammationListeria monocytogenesListeriosisLymphocyte ActivationMiceAntigens, CDApyraseCD39 antigen

Identifiers

PMID29742141
PMCPMC5942830
OpenAlexW2802665663

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.