Evidence map›Paper›PMID 31417563›Full record

ArticleFrontiers in immunology2019

Overexpression of PDE4A Acts as Checkpoint Inhibitor Against cAMP-Mediated Immunosuppression

Klaus G Schmetterer, Katrin Goldhahn, Liesa S Ziegler, Marlene C Gerner, Ralf L J Schmidt, Madeleine Themanns, Eva Zebedin-Brandl, Doris Trapin, Judith Leitner, Winfried F Pickl and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 18 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

13 authors at 1 institution in 1 country.

Klaus G SchmettererDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Katrin GoldhahnDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Liesa S ZieglerDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Marlene C GernerDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Ralf L J SchmidtDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Madeleine ThemannsCenter of Physiology and Pharmacology, Institute of Pharmacology, Medical University of Vienna, Vienna, Austria.
Eva Zebedin-BrandlCenter of Physiology and Pharmacology, Institute of Pharmacology, Medical University of Vienna, Vienna, Austria.
Doris TrapinCenter for Pathophysiology, Infectiology and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Judith LeitnerCenter for Pathophysiology, Infectiology and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Winfried F PicklCenter for Pathophysiology, Infectiology and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Peter SteinbergerCenter for Pathophysiology, Infectiology and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Ilse SchwarzingerDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Rodrig MarculescuDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · AT

Funding

Austrian Science Fund FWF P 29654
6 · The paper itself

Abstract

Malignant cells acquire physiological mechanisms of immunosuppression to escape immune surveillance. Strategies to counteract this suppression could help to improve adoptive immunotherapy regimen. The intracellular second messenger cyclic AMP (cAMP) acts as a potent immunosuppressive signaling molecule in T-cells and is up-regulated by multiple tumor-relevant suppressive factors including prostaglandin E2 (PGE2), adenosine and the functions of regulatory T-cells. Consequently, we aimed to abrogate cAMP signaling in human T-cells by ectopic overexpression of phosphodiesterase 4A (PDE4A). We could show that retroviral transduction of PDE4A into T-cells led to efficient degradation of cAMP in response to induction of adenylate cyclase. Retroviral transduction of PDE4A into CD4

Indexed as

Immune ToleranceCD8-Positive T-LymphocytesCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4DinoprostoneGene Expression Regulation, EnzymologicHEK293 CellsHumansT-Lymphocytes, RegulatoryCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4DinoprostonePDE4A protein, humanadoptive immunotherapycheckpoint inhibitorimmune toleranceT-cell engineeringtumor immunosuppression

Identifiers

PMID31417563
PMCPMC6682678
OpenAlexW2956238356

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.