Evidence map›Paper›PMID 24416207›Full record

ArticlePloS one2014

Bridging the species divide: transgenic mice humanized for type-I interferon response.

Daniel Harari, Renne Abramovich, Alla Zozulya, Paul Smith, Sandrine Pouly, Mario Köster, Hansjörg Hauser, Gideon Schreiber

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Structure-function of type I and III interferons.Current opinion in immunology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 3 institutions in 3 countries.

Daniel HarariDepartment of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
Renne AbramovichDepartment of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
Alla ZozulyaMS Platform, Merck-Serono, (a division of Merck KGaA), Geneva, Switzerland.
Paul SmithMS Platform, Merck-Serono, (a division of Merck KGaA), Geneva, Switzerland.
Sandrine PoulyMS Platform, Merck-Serono, (a division of Merck KGaA), Geneva, Switzerland.
Mario KösterHelmholtz Centre for Infection Research, Dept. Gene Regulation and Differentiation, Braunschweig, Germany.
Hansjörg HauserHelmholtz Centre for Infection Research, Dept. Gene Regulation and Differentiation, Braunschweig, Germany.
Gideon SchreiberDepartment of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
Merck Serono (Switzerland) · CHWeizmann Institute of Science · ILHelmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have generated transgenic mice that harbor humanized type I interferon receptors (IFNARs) enabling the study of type I human interferons (Hu-IFN-Is) in mice. These "HyBNAR" (Hybrid IFNAR) mice encode transgenic variants of IFNAR1 and IFNAR2 with the human extracellular domains being fused to transmembrane and cytoplasmic segments of mouse sequence. B16F1 mouse melanoma cells harboring the HyBNAR construct specifically bound Hu-IFN-Is and were rendered sensitive to Hu-IFN-I stimulated anti-proliferation, STAT1 activation and activation of a prototypical IFN-I response gene (MX2). HyBNAR mice were crossed with a transgenic strain expressing the luciferase reporter gene under the control of the IFN-responsive MX2 promoter (MX2-Luciferase). Both the HyBNAR and HyBNAR/MX2-Luciferase mice were responsive to all Hu-IFN-Is tested, inclusive of IFNα2A, IFNβ, and a human superagonist termed YNSα8. The mice displayed dose-dependent pharmacodynamic responses to Hu-IFN-I injection, as assessed by measuring the expression of IFN-responsive genes. Our studies also demonstrated a weak activation of endogenous mouse interferon response, especially after high dose administration of Hu-IFNs. In sharp contrast to data published for humans, our pharmacodynamic readouts demonstrate a very short-lived IFN-I response in mice, which is not enhanced by sub-cutaneous (SC) injections in comparison to other administration routes. With algometric differences between humans and mice taken into account, the HyBNAR mice provides a convenient non-primate pre-clinical model to advance the study of human IFN-Is.

Indexed as

AnimalsCell LineHomozygoteHumansInterferon Type ILuciferasesMelanoma, ExperimentalMiceMice, Inbred C57BLMice, TransgenicSignal TransductionSpecies SpecificityTransfectionTransgenesInterferon Type ILuciferases

Identifiers

PMID24416207
PMCPMC3887009
OpenAlexW2039434577

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.