Evidence map›Paper›PMID 31749798›Full record

ArticleFrontiers in immunology2019

The NF-κB RelA Transcription Factor Is Critical for Regulatory T Cell Activation and Stability.

Emilie Ronin, Martina Lubrano di Ricco, Romain Vallion, Jordane Divoux, Ho-Keun Kwon, Sylvie Grégoire, Davi Collares, Angéline Rouers, Véronique Baud, Christophe Benoist and 1 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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 51 citations in OpenAlex.

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  14. New insights into the Lck-NF-κB signaling pathway.Frontiers in cell and developmental biology · 2023
    Review
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  17. Patients With Severe Multiple Sclerosis Exhibit Functionally Altered CD8Neurology(R) neuroimmunology & neuroinflammation · 2022
    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

11 authors at 3 institutions in 2 countries.

Emilie RoninSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Martina Lubrano di RiccoSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Romain VallionSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Jordane DivouxSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Ho-Keun KwonDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, United States.
Sylvie GrégoireSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Davi CollaresLaboratoire NF-κB, Differentiation and Cancer, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Angéline RouersSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Véronique BaudLaboratoire NF-κB, Differentiation and Cancer, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Christophe BenoistDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, United States.
Benoit L SalomonSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France.
Centre National de la Recherche Scientifique · FRDélégation Paris 5 · FRHarvard University · US

Funding

Specification of Treg cells: FOXP3 functional facetsR01AI116834 · NIAID · HARVARD MEDICAL SCHOOL · PI BENOIST, CHRISTOPHE O. · 2015 to 2019
$2.3M
NIAID NIH HHS R01 AI116834
6 · The paper itself

Abstract

Regulatory T cells (Tregs) play a major role in immune homeostasis and in the prevention of autoimmune diseases. It has been shown that c-Rel is critical in Treg thymic differentiation, but little is known on the role of NF-κB on mature Treg biology. We thus generated mice with a specific knockout of RelA, a key member of NF-κB, in Tregs. These mice developed a severe autoimmune syndrome with multi-organ immune infiltration and high activation of lymphoid and myeloid cells. Phenotypic and transcriptomic analyses showed that RelA is critical in the acquisition of the effector Treg state independently of surrounding inflammatory environment. Unexpectedly, RelA-deficient Tregs also displayed reduced stability and cells that had lost Foxp3 produced inflammatory cytokines. Overall, we show that RelA is critical for Treg biology as it promotes both the generation of their effector phenotype and the maintenance of their identity.

Indexed as

ImmunomodulationAnimalsBiomarkersCytokinesGene Expression RegulationImmunophenotypingLymphocyte ActivationMiceMice, KnockoutT-Lymphocytes, RegulatoryT-Lymphocyte SubsetsTranscription Factor RelABiomarkersCytokinesTranscription Factor RelAactivationautoimmunityNF-κBregulatory T cellsrelAstability

Identifiers

PMID31749798
PMCPMC6842949
OpenAlexW2982416797

What OpenQuestion holds

Textmetadata
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.