Evidence map›Paper›PMID 19040572›Full record

ArticleCell proliferation2008

Regulation of apoptosis by type III interferons.

W Li, A Lewis-Antes, J Huang, M Balan, S V Kotenko

Abstract read
In one paragraph

Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed, 97 citations in OpenAlex.

  1. Type I-interferon β induces a strong anti-tumour response in bladder cancer cells.Journal of cancer research and clinical oncology · 2026
    Article
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  15. Review
  16. Targeting IL-10 Family Cytokines for the Treatment of Human Diseases.Cold Spring Harbor perspectives in biology · 2019
    Review
  17. Article
  18. Article
  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

5 authors at 2 institutions in 1 country.

W LiDepartment of Biochemistry and Molecular Biology, New Jersey Medical School-University Hospital Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
A Lewis-AntesDepartment of Biochemistry and Molecular Biology, New Jersey Medical School-University Hospital Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
J HuangDepartment of Biochemistry and Molecular Biology, New Jersey Medical School-University Hospital Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
M BalanDepartment of Biochemistry and Molecular Biology, New Jersey Medical School-University Hospital Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
S V KotenkoDepartment of Biochemistry and Molecular Biology, New Jersey Medical School-University Hospital Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
Rutgers New Jersey Medical SchoolUniversity Hospital, Newark · US

Funding

Role of Interferon-lambda in Antiviral ResponseR01AI057468 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KOTENKO, SERGEI V · 2005 to 2009
$1.9M
Characterization of the IL-TIF Receptor ComplexR01AI051139 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KOTENKO, SERGEI V · 2001 to 2005
$1.4M
NIAID NIH HHS AI057468NIAID NIH HHS R01 AI051139NIAID NIH HHS R01 AI057468
6 · The paper itself

Abstract

objectiveTwo types of interferons (IFNs), type I (IFN-alpha/beta) and type III (IFN-lambdas), utilize distinct receptor complexes to induce similar signalling and biological activities, including recently demonstrated for IFN-lambdas antitumour activity. However, ability of type III IFNs to regulate cell population growth remains largely uncharacterized. MATERIALS AND

methodsIntact and modified human colorectal adenocarcinoma HT29 cells were used to study regulation of apoptosis by IFN-lambdas. RESULTS AND

conclusionsWe report that the IFN-lambdaR1 chain of the type III IFN receptor complex possesses an intrinsic ability to trigger apoptosis in cells. Signalling induced through the intracellular domain of IFN-lambdaR1 resulted in G(1)/G(0) phase cell cycle arrest, phosphatidylserine surfacing and chromosomal DNA fragmentation. Caspase-3, caspase-8 and caspase-9 were activated; however, pancaspase inhibitor Z-VAD-FMK did not prevent apoptosis. In addition, the extent of apoptosis correlated with the level of receptor expression and was associated with prolonged IFN-lambda signalling. We also demonstrated that the ability to trigger apoptosis is a unique intrinsic function of all IFN receptors. However, more robust apoptosis was induced by signalling through type III IFN receptor than through type I or type II (IFN-gamma) receptors, suggesting higher cytotoxic potential of type III IFNs. In addition, we observed that IFN-gamma treatment sensitized HT29 cells to IFN-lambda-mediated apoptosis. These results provide evidence that type III IFNs, alone or in combination with other stimuli, have the potential to induce apoptosis.

Indexed as

ApoptosisCaspasesCell CycleCell Line, TumorDNA FragmentationEnzyme ActivationHumansInterferonsPhosphatidylserinesReceptors, InterferonSignal TransductionSTAT1 Transcription FactorCaspasesInterferonsPhosphatidylserinesReceptors, InterferonSTAT1 Transcription Factor

Identifiers

PMID19040572
PMCPMC6496378
OpenAlexW2132439466

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.