Evidence map›Paper›PMID 26692072›Full record

ArticleEuropean journal of immunology2016

Characterization of a conditional interleukin-1 receptor 1 mouse mutant using the Cre/LoxP system.

Wesam H Abdulaal, Catherine R Walker, Ryan Costello, Elena Redondo-Castro, Ilgiz A Mufazalov, Athina Papaemmanouil, Nancy J Rothwell, Stuart M Allan, Ari Waisman, Emmanuel Pinteaux and 1 more

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  12. Cutting Edge: IL-1R1 Mediates Host Resistance toJournal of immunology (Baltimore, Md. : 1950) · 2018
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  13. Article
  14. Cardiac fibroblast-specific p38α MAP kinase promotes cardiac hypertrophy via a putative paracrine interleukin-6 signaling mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
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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

11 authors at 3 institutions in 3 countries.

Wesam H AbdulaalFaculty of Life Sciences, University of Manchester, Manchester, UK.
Catherine R WalkerFaculty of Life Sciences, University of Manchester, Manchester, UK.
Ryan CostelloFaculty of Life Sciences, University of Manchester, Manchester, UK.
Elena Redondo-CastroFaculty of Life Sciences, University of Manchester, Manchester, UK.
Ilgiz A MufazalovInstitute for Molecular Medicine, Medical University of Johannes Gutenberg-University of Mainz, Mainz, Germany.
Athina PapaemmanouilFaculty of Life Sciences, University of Manchester, Manchester, UK.
Nancy J RothwellFaculty of Life Sciences, University of Manchester, Manchester, UK.
Stuart M AllanFaculty of Life Sciences, University of Manchester, Manchester, UK.
Ari WaismanInstitute for Molecular Medicine, Medical University of Johannes Gutenberg-University of Mainz, Mainz, Germany.
Emmanuel PinteauxFaculty of Life Sciences, University of Manchester, Manchester, UK.
Werner MüllerFaculty of Life Sciences, University of Manchester, Manchester, UK.
University of Manchester · GBJohannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

Biotechnology and Biological Sciences Research Council BB/I016333/1British Heart Foundation PG/13/55/30365British Heart Foundation PG/13/8/29989Medical Research Council G0801296
6 · The paper itself

Abstract

IL-1 is a key cytokine known to drive chronic inflammation and to regulate many physiological, immunological, and neuroimmunological responses via actions on diverse cell types of the body. To determine the mechanisms of IL-1 actions as part of the inflammatory response in vivo, we generated a conditional IL-1 receptor 1 (IL-1R1) mouse mutant using the Cre/LoxP system (IL-1R1(fl/fl) ). In the mutant generated, exon 5, which encodes part of the extracellular-binding region of the receptor, is flanked by LoxP sites, thereby inactivating the two previously described functional IL-1R1 gene transcripts after Cre-mediated recombination. Using keratin 14-Cre driver mice, new IL-1R1 deficient (-/-) mice were subsequently generated, in which all signaling IL-1 receptor isoforms are deleted ubiquitously. Furthermore, using vav-iCre driver mice, we deleted IL-1 receptor isoforms in the hematopoietic system. In these mice, we show that both the IL-17 and IL-22 cytokine response is reduced, when mice are challenged by the helminth Trichuris muris. We are currently crossing IL-1R1(fl/fl) mice with different Cre-expressing mice in order to study mechanisms of acute and chronic inflammatory diseases.

Indexed as

AnimalsInflammationInterleukin-17Interleukin-22InterleukinsKeratin-14MiceMice, Inbred C57BLMice, KnockoutReceptors, Interleukin-1 Type ITrichurisIl17a protein, mouseIL1R1 protein, mouseInterleukin-17Interleukin-22InterleukinsKeratin-14Krt14 protein, mouseReceptors, Interleukin-1 Type ICre/loxPIL-17Immune regulationInfectionTrichuris muris

Identifiers

PMID26692072
PMCPMC4982085
OpenAlexW2208937711

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.