Evidence map›Paper›PMID 18203138›Full record

ArticleEuropean journal of immunology2008

Opposing regulation of T cell function by Egr-1/NAB2 and Egr-2/Egr-3.

Sam Collins, Michael A Lutz, Paul E Zarek, Robert A Anders, Gilbert J Kersh, Jonathan D Powell

Abstract read
In one paragraph

Article in European journal of immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

69 citing papers in PubMed, 108 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Dendritic cell PD-L2 restrains intratumoral CD8bioRxiv : the preprint server for biology · 2026
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  7. Frontiers in pharmacology · 2026
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Cytolytic CD8Science immunology · 2023
    Article
  15. Inducible CRISPR Epigenome Systems Mimic Cocaine Induced Bidirectional Regulation of Nab2 and Egr3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Sam CollinsThe Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Michael A Lutz
Paul E Zarek
Robert A Anders
Gilbert J Kersh
Jonathan D Powell
Johns Hopkins University · USSidney Kimmel Comprehensive Cancer Center · USEmory University · US

Funding

EGR-2/3 and NAB2 in T Cell Anergy and ActivationR01CA098109 · NCI · JOHNS HOPKINS UNIVERSITY · PI POWELL, JONATHAN D · 2003 to 2013
$2.5M
NCI NIH HHS R01 CA098109NCI NIH HHS R01 CA 098109-02
6 · The paper itself

Abstract

TCR-induced NF-AT activation leads to the up-regulation of multiple genes involved in T cell anergy. Since NF-AT is also involved in T cell activation, we have endeavored to dissect TCR-induced activating and inhibitory genetic programs. This approach revealed roles for the early growth response (Egr) family of transcription factors and the Egr coactivator/corepressor NGFI-A-binding protein (NAB)2 in regulating T cell function. TCR-induced Egr-1 and NAB2 enhance T cell function, while Egr-2 and Egr-3 inhibit T cell function. In this report, we demonstrate that Egr-2 and Egr-3 are induced by NF-AT in the absence of AP-1, while Egr-1 and NAB2 both require AP-1-mediated transcription. Our data suggest that Egr-3 is upstream of Egr-2, and that mechanistically Egr-2 and Egr-3 suppress Egr-1 and NAB2 expression. Functionally, T cells from Egr-2 and Egr-3 null mice are hyperresponsive while T cells from Egr-3 transgenic, overexpressing mice are hyporesponsive. Furthermore, an in vivo model of autoimmune pneumonitis reveals that T cells from Egr-3 null mice hasten death while Egr-3-overexpressing T cells cause less disease. Overall, our data suggest that just as the Egr/NAB network of genes control cell fate in other systems, TCR-induced Egr-1, 2, 3 and NAB2 control the fate of antigen recognition in T cells.

Indexed as

AnimalsEarly Growth Response Protein 1Early Growth Response Protein 2Early Growth Response Protein 3Gene Expression RegulationMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicNeoplasm ProteinsReceptors, Antigen, T-CellRepressor ProteinsT-LymphocytesEarly Growth Response Protein 1Early Growth Response Protein 2Early Growth Response Protein 3Egr1 protein, mouseEgr2 protein, mouseEgr3 protein, mouseNab2 protein, mouseNeoplasm ProteinsReceptors, Antigen, T-CellRepressor Proteins

Identifiers

PMID18203138
PMCPMC3598016
OpenAlexW1996493268

What OpenQuestion holds

Textmetadata
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.