Evidence map›Paper›PMID 24597649›Full record

ArticleImmunology2014

Critical role of the endogenous interferon ligand-receptors in type I and type II interferons response.

Ahmed Lasfar, Jeffry R Cook, Karine A Cohen Solal, Kenneth Reuhl, Sergei V Kotenko, Jerome A Langer, Debra L Laskin

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2014. 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
0.6field-weighted citation impact, top 32% 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, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 3CVirologica Sinica · 2023
    Article
  5. Article
  6. Review
  7. Theranostics · 2020
    Article
  8. Article
  9. Comprehensive network map of interferon gamma signaling.Journal of cell communication and signaling · 2018
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
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

7 authors at 2 institutions in 1 country.

Ahmed LasfarDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers, the State University of New Jersey, Piscataway, NJ, USA; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.
Jeffry R Cook
Karine A Cohen Solal
Kenneth Reuhl
Sergei V Kotenko
Jerome A Langer
Debra L Laskin
Rutgers, The State University of New Jersey · USRutgers Cancer Institute of New Jersey

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
UMDNJ/Rutgers University CounterACT Research Center of ExcellenceU54AR055073 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HECK, DIANE E · 2006 to 2024
$71.4M
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
ACTIVATED MACROPHAGES AND OZONE TOXICITYR01ES004738 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Debra L Laskin · 1989 to 2026
$9.0M
Macrophages and Inflammatory Mediators in Silica-Induced CarcinogenesisR01CA132624 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI LASKIN, DEBRA L · 2008 to 2012
$1.5M
NCI NIH HHS CA132624NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA132624NIAMS NIH HHS AR055073NIAMS NIH HHS U54 AR055073NIEHS NIH HHS ES004738NIEHS NIH HHS ES005022NIEHS NIH HHS P30 ES005022NIEHS NIH HHS R01 ES004738PHS HHS R01 051139
6 · The paper itself

Abstract

Separate ligand-receptor paradigms are commonly used for each type of interferon (IFN). However, accumulating evidence suggests that type I and type II IFNs may not be restricted to independent pathways. Using different cell types deficient in IFNAR1, IFNAR2, IFNGR1, IFNGR2 and IFN-γ, we evaluated the contribution of each element of the IFN system to the activity of type I and type II IFNs. We show that deficiency in IFNAR1 or IFNAR2 is associated with impairment of type II IFN activity. This impairment, presumably resulting from the disruption of the ligand-receptor complex, is obtained in all cell types tested. However, deficiency of IFNGR1, IFNGR2 or IFN-γ was associated with an impairment of type I IFN activity in spleen cells only, correlating with the constitutive expression of type II IFN (IFN-γ) observed on those cells. Therefore, in vitro the constitutive expression of both the receptors and the ligands of type I or type II IFN is critical for the enhancement of the IFN activity. Any IFN deficiency can totally or partially impair IFN activity, suggesting the importance of type I and type II IFN interactions. Taken together, our results suggest that type I and type II IFNs may regulate biological activities through distinct as well as common IFN receptor complexes.

Indexed as

AnimalsInterferon-gammaInterferon Type ILigandsMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutReceptor, Interferon alpha-betaIfnar1 protein, mouseIfnar2 protein, mouseInterferon-gammaInterferon Type ILigandsReceptor, Interferon alpha-betacell typesconstitutive interferoninterferon receptor paradigminterferon responseT cellstype I and type II interferon receptors

Identifiers

PMID24597649
PMCPMC4080960
OpenAlexW2009474968

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.