Evidence map›Paper›PMID 29314730›Full record

ArticleImmunity, inflammation and disease2018

Transcription factors early growth response gene (Egr) 2 and 3 control inflammatory responses of tolerant T cells.

Becky Omodho, Tizong Miao, Alistair L J Symonds, Randeep Singh, Suling Li, Ping Wang

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.1field-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

8 citing papers in PubMed, 30 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Becky OmodhoThe Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, UK.
Tizong MiaoThe Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, UK.
Alistair L J SymondsThe Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, UK.ORCID 0000-0002-9461-0816
Randeep SinghBioscience, Brunel University London, Kingston Lane, London, UK.
Suling LiBioscience, Brunel University London, Kingston Lane, London, UK.
Ping WangThe Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, UK.
Queen Mary University of London · GBKingston University · GB

Funding

Arthritis Research UKMedical Research Council MR/N00096X/1Versus Arthritis 20455
6 · The paper itself

Abstract

introductionImpaired proliferation and production of IL2 are the hallmarks of experimental T cell tolerance. However, in most autoimmune diseases, auto-reactive T cells do not display hyper proliferation, but inflammatory phenotypes.

methodsWe have now demonstrated that the transcription factors Egr2 and 3 are important for the control of inflammatory cytokine production by tolerant T cells, but not for tolerance induction.

resultsIn the absence of Egr2 and 3, T cell tolerance, as measured by impaired proliferation and production of IL2, can still be induced, but tolerant T cells produced high levels of inflammatory cytokines. Egr2 and 3 regulate expression of differentiation repressors and directly inhibit T-bet function in T cells. Indeed, decreased expression of differentiation repressors, such as Id3 and Tcf1, and increased expression of inflammatory transcription factors, such as RORγt and Bhlhe40 were found in Egr2/3 deficient T cells under tolerogenic conditions. In addition, T-bet was co-expressed with Egr2 in tolerant T cells and Egr2/3 defects leads to production of high levels of IFNγ in tolerant T cells.

conclusionsOur findings demonstrated that despite impaired proliferation and IL2 production, tolerant T cells can display inflammatory responses in response to antigen stimulation and this is controlled at least partly by Egr2 and 3.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteAutoantigensBone Marrow TransplantationCD2 AntigensCD69 AntigensCell ProliferationDisease Models, AnimalEarly Growth Response Protein 2Early Growth Response Protein 3EnterotoxinsGene Expression RegulationGene Knock-In TechniquesHumansHyaluronan ReceptorsAntigens, CDAntigens, Differentiation, T-LymphocyteAutoantigensCD2 AntigensCd44 protein, mouseCD69 AntigensEarly Growth Response Protein 2Early Growth Response Protein 3Egr2 protein, mouseEgr3 protein, mouseenterotoxin A, StaphylococcalEnterotoxinsHyaluronan ReceptorsInterleukin-2Lectins, C-TypeEgr2T cellstolerance

Identifiers

PMID29314730
PMCPMC5946152
OpenAlexW2782203211

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Registered trials

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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.