Evidence map›Paper›PMID 15964802›Full record

ArticleMolecular and cellular biology2005

Stat1 and Stat2 but not Stat3 arbitrate contradictory growth signals elicited by alpha/beta interferon in T lymphocytes.

Ramon Gimeno, Chien-Kuo Lee, Christian Schindler, David E Levy

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. IL-27 promotes the expansion of self-renewing CD8The Journal of experimental medicine · 2019
    Article
  9. Review
  10. Type I Interferons Interfere with the Capacity of mRNA Lipoplex Vaccines to Elicit Cytolytic T Cell Responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Article
  11. Review
  12. Type I interferons in infectious disease.Nature reviews. Immunology · 2015
    Review
  13. Host STAT2/type I interferon axis controls tumor growth.International journal of cancer · 2015
    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 2 institutions in 1 country.

Ramon GimenoDepartment of Pathology and Microbiology, 550 First Ave. MSB548, New York University School of Medicine, New York, New York 10016, USA.
Chien-Kuo Lee
Christian Schindler
David E Levy
New York University · USColumbia University · US

Funding

SIGNAL TRANSDUCTION PATHWAY IN IFN INDUCED TRANSCRIPTIONR01AI028900 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LEVY, DAVID E · 1990 to 2010
$5.6M
VIRUS INDUCED DC MATURATION AND CELLULAR IMMUNITYP01AI048204 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI PALESE, PETER · 2000 to 2003
$3.8M
NIAID NIH HHS P01 AI048204NIAID NIH HHS R01 AI028900
6 · The paper itself

Abstract

Alpha/beta interferon (IFN-alpha/beta) triggers antiviral and antiproliferative responses in target cells through modulation of gene expression. The JAK-STAT pathway is the major mediator of these biological effects through the activation of the transcription factors STAT1 and STAT2, and gene ablation studies have demonstrated that both STAT1 and STAT2 are required for most antiviral responses induced by IFN-alpha/beta. However, additional signaling pathways are also activated by IFN. Here, we show that these additional pathways provoke a proliferative response in activated T lymphocytes. While activation of IFN-stimulated gene factor 3 produces a dominant inhibitory signal capable of overriding the mitogenic response, absence of either STAT1 or STAT2 leads to a proliferative response to IFN. Growth stimulation by IFN-alpha/beta is independent of other STAT proteins, particularly of STAT3, since T lymphocytes from STAT1-STAT3 double-knockout mice are growth stimulated by IFN-alpha/beta treatment. IFN-alpha/beta can cooperate with numerous T-cell mitogens, including interleukin-2 (IL-2), IL-4, IL-7, and IL-12, and can contribute to the rapid restoration of the thymus following glucocorticoid-mediated ablation. These results underscore the complexity of the cellular response to IFN and suggest that the ultimate outcome of IFN action results from a balance between growth-inhibitory and -stimulatory effects.

Indexed as

AnimalsCell ProliferationCells, CulturedCrosses, GeneticDNA-Binding ProteinsFlow CytometryInterferon-alphaInterferon-betaInterleukin-2MiceMice, Inbred StrainsMice, TransgenicProteinsSignal TransductionSpleenSTAT1 Transcription FactorDNA-Binding ProteinsInterferon-alphaInterferon-betaInterleukin-2ProteinsStat1 protein, mouseSTAT1 Transcription FactorStat2 protein, mouseSTAT2 Transcription FactorStat3 protein, mouseSTAT3 Transcription FactorTrans-Activators

Identifiers

PMID15964802
PMCPMC1156979
OpenAlexW2138887560

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.