Evidence map›Paper›PMID 32205878›Full record

ArticleNature immunology2020

A molecular network regulating the proinflammatory phenotype of human memory T lymphocytes.

Stefan Emming, Niccolò Bianchi, Sara Polletti, Chiara Balestrieri, Cristina Leoni, Sara Montagner, Michele Chirichella, Nicolas Delaleu, Gioacchino Natoli, Silvia Monticelli

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.5field-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

46 citing papers in PubMed, 76 citations in OpenAlex.

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  13. RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024
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  19. Steady-state memory-phenotype conventional CD4Experimental & molecular medicine · 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

10 authors at 5 institutions in 3 countries.

Stefan Emming *Institute for Research in Biomedicine, Università della Svizzera Italiana (USI), Bellinzona, Switzerland.ORCID http://orcid.org/0000-0002-3851-335X
Niccolò Bianchi *Institute for Research in Biomedicine, Università della Svizzera Italiana (USI), Bellinzona, Switzerland.
Sara Polletti *Department of Experimental Oncology, European Institute of Oncology IRCCS (IEO), Milan, Italy.
Chiara BalestrieriDepartment of Experimental Oncology, European Institute of Oncology IRCCS (IEO), Milan, Italy.
Cristina LeoniInstitute for Research in Biomedicine, Università della Svizzera Italiana (USI), Bellinzona, Switzerland.
Sara MontagnerInstitute for Research in Biomedicine, Università della Svizzera Italiana (USI), Bellinzona, Switzerland.
Michele ChirichellaInstitute for Research in Biomedicine, Università della Svizzera Italiana (USI), Bellinzona, Switzerland.
Nicolas DelaleuInstitute of Oncology Research, Oncology Institute of Southern Switzerland, USI, Bellinzona, Switzerland.
Gioacchino NatoliDepartment of Experimental Oncology, European Institute of Oncology IRCCS (IEO), Milan, Italy.
Silvia MonticelliInstitute for Research in Biomedicine, Università della Svizzera Italiana (USI), Bellinzona, Switzerland. silvia.monticelli@irb.usi.ch.ORCID http://orcid.org/0000-0002-5909-8802
Università della Svizzera italiana · CHEuropean Institute of Oncology · ITUniversity of Bern · CHHumanitas University · ITInstitute of Oncology Research · CH

Funding

Swiss National Science Foundation 156875
6 · The paper itself

Abstract

Understanding the mechanisms that modulate helper T lymphocyte functions is crucial to decipher normal and pathogenic immune responses in humans. To identify molecular determinants influencing the pathogenicity of T cells, we separated ex vivo-isolated primary human memory T lymphocytes on the basis of their ability to produce high levels of inflammatory cytokines. We found that the inflammatory, cytokine-producing phenotype of memory T lymphocytes was defined by a specific core gene signature and was mechanistically regulated by the constitutive activation of the NF-κB pathway and by the expression of the transcriptional repressor BHLHE40. BHLHE40 attenuated the expression of anti-inflammatory factors, including miR-146a, a negative regulator of NF-κB activation and ZC3H12D, an RNase of the Regnase-1 family able to degrade inflammatory transcripts. Our data reveal a molecular network regulating the proinflammatory phenotype of human memory T lymphocytes, with the potential to contribute to disease.

Indexed as

Cell LineCell Line, TumorCytokinesGene Expression RegulationHEK293 CellsHumansImmunologic MemoryInflammationJurkat CellsLymphocyte ActivationNF-kappa BPhenotypeT-LymphocytesCytokinesNF-kappa B

Identifiers

PMID32205878
PMCPMC7100912
OpenAlexW3011105477

What OpenQuestion holds

Textmetadata
LicenceTDM
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.