Evidence map›Paper›PMID 14560009›Full record

ArticleMolecular and cellular biology2003

Egr family members regulate nonlymphoid expression of Fas ligand, TRAIL, and tumor necrosis factor during immune responses.

Nathalie M Droin, Michael J Pinkoski, Emmanuel Dejardin, Douglas R Green

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-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

27 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Nathalie M DroinDivision of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, California 92121, USA.
Michael J Pinkoski
Emmanuel Dejardin
Douglas R Green
La Jolla Institute for Immunology · US

Funding

Survival Function of the Fadd-Caspase-8-Flip ComplexR01AI044828 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GREEN, DOUGLAS R. · 1999 to 2016
$6.3M
Survival Function of the Fadd-Caspase-8-Flip Complex - MERIT ExtensionR37AI044828 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Douglas R. Green · 2017 to 2026
$4.5M
NIAID NIH HHS AI44828NIAID NIH HHS R01 AI044828NIAID NIH HHS R37 AI044828
6 · The paper itself

Abstract

The Fas ligand (FasL)/Fas pathway is crucial for homeostasis of the immune system and peripheral tolerance. Peripheral lymphocyte deletion involves FasL/Fas in at least two ways: coexpression of both Fas and its ligand on T cells, leading to activation-induced cell death, and expression of FasL by nonlymphoid cells, such as intestinal epithelial cells (IEC), that kill Fas-positive T cells. We demonstrate here that superantigen Staphylococcus enterotoxin B (SEB) induced a dramatic upregulation of FasL, TRAIL, and TNF mRNA expression and function in IEC from BALB/c and C57BL/6 mice. Using adoptive transfer in which CD4(+) T cells from OT-2 T-cell receptor transgenic mice were transferred into recipients, we observed an induction in IEC of FasL, TRAIL, and TNF mRNA after administration of antigen. Specific Egr-binding sites have been identified in the 5' promoter region of the FasL gene, and Egr-1, Egr-2, and Egr-3 mRNA in IEC from mice treated with SEB and from transgenic OT-2 mice after administration of antigen was upregulated. Overexpression of Egr-2 and Egr-3 induced endogenous ligand upregulation that was inhibited by overexpression of Egr-specific inhibitor Nab1. These results support a role for Egr family members in nonlymphoid expression of FasL, TRAIL, and TNF.

Indexed as

Gene Expression RegulationAdoptive TransferAnimalsAntigens, BacterialAntigens, CDApoptosis Regulatory ProteinsCD4-Positive T-LymphocytesDNA-Binding ProteinsEarly Growth Response Protein 1Early Growth Response Protein 2Early Growth Response Protein 3EnterotoxinsEpithelial CellsFas Ligand ProteinHumansImmediate-Early ProteinsAntigens, BacterialAntigens, CDApoptosis Regulatory ProteinsDNA-Binding ProteinsEarly Growth Response Protein 1Early Growth Response Protein 2Early Growth Response Protein 3EGR1 protein, humanEgr1 protein, mouseEGR2 protein, humanEgr2 protein, mouseEgr3 protein, mouseenterotoxin B, staphylococcalEnterotoxinsFASLG protein, humanFas Ligand ProteinFasl protein, mouseImmediate-Early ProteinsMembrane GlycoproteinsNAB1 protein, humanNab1 protein, mouseReceptors, Antigen, T-CellReceptors, TNF-Related Apoptosis-Inducing LigandReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IRepressor ProteinsRNA, MessengerTNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, humanTnfrsf10b protein, mouseTNFSF10 protein, humanTnfsf10 protein, mouseTranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID14560009
PMCPMC207583
OpenAlexW2111784784

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.