Evidence map›Paper›PMID 18779345›Full record

ArticleThe Journal of experimental medicine2008

Early growth response gene 2 (Egr-2) controls the self-tolerance of T cells and prevents the development of lupuslike autoimmune disease.

Bo Zhu, Alistair L J Symonds, Joanne E Martin, Dimitris Kioussis, David C Wraith, Suling Li, Ping Wang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.2field-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

59 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  8. From bench to bedside: targeting lymphocyte activation gene 3 as a therapeutic strategy for autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  9. CARD19, a Novel Regulator of the TAK1/NF-κB Pathway in Self-Reactive B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  10. Article
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  18. Reevaluation of Pluripotent Cytokine TGF-β3 in Immunity.International journal of molecular sciences · 2018
    Review
  19. Article
  20. Article
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

7 authors at 4 institutions in 1 country.

Bo ZhuInstitute of Cell and Molecular Science, Barts and London School of Medicine and Dentistry, University of London, London E1 2AT, England, UK.
Alistair L J Symonds
Joanne E Martin
Dimitris Kioussis
David C Wraith
Suling Li
Ping Wang
Queen Mary University of London · GBBrunel University of London · GBMedical Research Council · GBUniversity of Bristol · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council MC_U117512796Wellcome Trust 074731
6 · The paper itself

Abstract

Maintaining tolerance of T cells to self-antigens is essential to avoid autoimmune disease. How self-reactive T cells are kept functionally inactive is, however, unknown. In this study, we show that early growth response gene 2 (Egr-2), a zinc-finger transcription factor, is expressed in CD44(high) T cells and controls their proliferation and activation. In the absence of Egr-2, CD44(high), but not CD44(low) T cells, are hyperreactive and hyperproliferative in vivo. The accumulation of activated CD4(+)CD44(high) T cells leads to the development of a late onset lupuslike autoimmune disease characterized by the accumulation of interferon (IFN)-gamma and interleukin (IL)-17-producing CD4(+) T cells, loss of tolerance to nuclear antigens, massive infiltration of T cells into multiple organs and glomerulonephritis. We found that the expression of cyclin-dependent kinase inhibitor p21cip1 was impaired in Egr-2-deficient T cells, whereas the expression of IFN-gamma and IL-17 in response to T cell receptor ligation was significantly increased, suggesting that Egr-2 activates the expression of genes involved in the negative regulation of T cell proliferation and inflammation. These results demonstrate that Egr-2 is an intrinsic regulator of effector T cells and controls the expansion of self-reactive T cells and development of autoimmune disease.

Indexed as

Autoimmune DiseasesSelf ToleranceAnimalsAutoantibodiesCell DifferentiationCell ProliferationCyclin-Dependent Kinase Inhibitor p21Early Growth Response Protein 2Hyaluronan ReceptorsInterleukin-2Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicSkinAutoantibodiesCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21Early Growth Response Protein 2Egr2 protein, mouseHyaluronan ReceptorsInterleukin-2

Identifiers

PMID18779345
PMCPMC2556781
OpenAlexW2161712070

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.