Evidence map›Paper›PMID 15249594›Full record

ArticleThe Journal of experimental medicine2004

Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells.

Michael Lohoff, Hans-Willi Mittrücker, Anne Brüstle, Frank Sommer, Bärbel Casper, Magda Huber, David A Ferrick, Gordon S Duncan, Tak W Mak

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Aloe-Emodin Ameliorates Diabetic Nephropathy by Targeting Interferon Regulatory Factor 4.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Transcription factor IRF4 determines germinal center formation through follicular T-helper cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  9. Article
  10. Article
  11. IRF4: Immunity. Malignancy! Therapy?Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Review
  12. Article
  13. Article
  14. 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

9 authors at 5 institutions in 3 countries.

Michael LohoffAdvanced Medical Discovery Institute, 620 University Ave, Suite 706, Toronto, Ontario, Canada M5G 2C1.
Hans-Willi Mittrücker
Anne Brüstle
Frank Sommer
Bärbel Casper
Magda Huber
David A Ferrick
Gordon S Duncan
Tak W Mak
Institut für Medizinische Informatik, Biometrie und Epidemiologie · DEDiscovery Institute · USMax Planck Institute for Infection Biology · DEUniversity of California, Davis · USUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factors of the interferon regulatory factor (IRF) family contribute to the regulation of cell proliferation and apoptosis. Here, we show that CD4(+) T helper (Th) cells lacking IRF4 (IRF4(-/-)) are highly sensitive to apoptosis. After infection of IRF4(-/-) mice with the protozoan parasite Leishmania major, the lesion-draining lymph nodes developed the prototypic lymphadenopathy of wild-type mice after 4 wk, but demonstrated almost total loss of cellularity and enhanced apoptosis after 7 wk. In vitro, activation of IRF4(-/-) CD4(+) Th cells led to greatly increased apoptosis compared with wild-type cells. Coculture of IRF4(-/-) and IRF4(+/+) CD4(+) cells did not increase survival of IRF4(-/-) CD4(+) cells, indicating that the enhanced rate of IRF4(-/-) Th cell apoptosis was neither transferable nor due to lack of a cytokine. Enhanced CD4(+) cell apoptosis was also observed after anti-CD95 mAb treatment, despite normal CD95 expression. Removal of endogenous cytokines, notably interleukin (IL)-4, led to increased and equally high levels of IRF4(-/-) and IRF4(+/+) cell apoptosis, whereas the protective activity of exogenous IL-4 was reduced in IRF4(-/-) CD4(+) cells despite normal expression of the IL-4 receptor. Therefore, IRF4 is central in protecting CD4(+) cells against proapoptotic stimuli.

Indexed as

ApoptosisAnimalsAnnexin A5CD4 AntigensCD4-Positive T-LymphocytesCell DivisionColoring AgentsCytokinesDNA-Binding Proteinsfas ReceptorFlow CytometryIn Situ Nick-End LabelingInterferon Regulatory Factor-4Interferon Regulatory FactorsLeishmania majorMiceAnnexin A5CD4 AntigensColoring AgentsCytokinesDNA-Binding Proteinsfas ReceptorInterferon Regulatory Factor-4Interferon Regulatory FactorsReceptors, Antigen, T-CellTranscription Factors

Identifiers

PMID15249594
PMCPMC2212018
OpenAlexW2098765637

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.