Evidence map›Paper›PMID 32468079›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2020

Cell-specific conditional deletion of interleukin-1 (IL-1) ligands and its receptors: a new toolbox to study the role of IL-1 in health and disease.

Emmanuel Pinteaux, Wesam H Abdulaal, Ilgiz A Mufazalov, Neil E Humphreys, Maj Simonsen-Jackson, Sheila Francis, Werner Müller, Ari Waisman

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. A CD4Immunity · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. 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 4 institutions in 4 countries.

Emmanuel PinteauxFaculty of Biology, Medicine and Health, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom. emmanuel.pinteaux@manchester.ac.uk.ORCID https://orcid.org/0000-0002-9986-4401
Wesam H AbdulaalFaculty of Biology, Medicine and Health, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom.
Ilgiz A MufazalovInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, Building 308A, 55131, Mainz, Germany.
Neil E HumphreysFaculty of Biology, Medicine and Health, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom.
Maj Simonsen-JacksonFaculty of Biology, Medicine and Health, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom.
Sheila FrancisDepartment of Infection, Immunity & Cardiovascular Disease, Medical School, University of Sheffield, S10 2RX, Sheffield, United Kingdom.
Werner MüllerFaculty of Biology, Medicine and Health, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom.
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, Building 308A, 55131, Mainz, Germany.
University of Manchester · GBJohannes Gutenberg University Mainz · DEKing Abdulaziz University · SAUniversity of Sheffield · GB

Funding

British Heart Foundation PG/13/55/30365Deutsche Forschungsgemeinschaft CRC1292Deutsche Forschungsgemeinschaft CRC/TRR128Seventh Framework Programme 305564
6 · The paper itself

Abstract

The pro-inflammatory cytokine interleukin-1 (IL-1) plays a key role in many physiological processes and during the inflammatory and immune response to most common diseases. IL-1 exists as two agonists, IL-1α and IL-1β that bind to the only signaling IL-1 type 1 receptor (IL-1R1), while a second decoy IL-1 type 2 receptor (IL-1R2) binds both forms of IL-1 without inducing cell signaling. The field of immunology and inflammation research has, over the past 35 years, unraveled many mechanisms of IL-1 actions, through in vitro manipulation of the IL-1 system or by using genetically engineered mouse models that lack either member of the IL-1 family in ubiquitous constitutive manner. However, the limitation of global mouse knockout technology has significantly hampered our understanding of the precise mechanisms of IL-1 actions in animal models of disease. Here we report and review the recent generation of new conditional mouse mutants in which exons of Il1a, Il1b, Il1r1, and Il1r2 genes flanked by loxP sites (

Indexed as

AnimalsHumansInflammationInterleukin-1LigandsReceptors, Interleukin-1Signal TransductionInterleukin-1LigandsReceptors, Interleukin-1Conditional deletionCre/loxPIL-1IL-1 receptorsImmunityInflammation

Identifiers

PMID32468079
PMCPMC7343756
OpenAlexW3031900093

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.