Evidence map›Paper›PMID 25409453›Full record

SynthesisPloS one2014

A candidate gene approach identifies an IL33 genetic variant as a novel genetic risk factor for GCA.

Ana Márquez, Roser Solans, José Hernández-Rodríguez, Maria C Cid, Santos Castañeda, Marc Ramentol, Luis Rodriguez-Rodriguez, Javier Narváez, Ricardo Blanco, Norberto Ortego-Centeno and 13 more

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Frontiers in immunology · 2021
    Article
  5. A single nucleotide polymorphism in theInternational journal of ophthalmology · 2021
    Article
  6. Article
  7. Review
  8. Review
  9. 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

23 authors at 17 institutions in 4 countries.

Ana MárquezInstituto de Parasitología y Biomedicina López-Neyra, CSIC, Granada, Spain; Systemic Autoimmune Diseases Unit, Hospital Clínico San Cecilio, Granada, Spain.
Roser SolansDepartment of Internal Medicine, Hospital Vall d'Hebron, Barcelona, Spain.
José Hernández-RodríguezVasculitis Research Unit, Department of Autoimmune and Systemic Diseases, Hospital Clinic, University of Barcelona, Centre de Recerca Biomèdica Cellex (IDIBAPS), Barcelona, Spain.
Maria C CidVasculitis Research Unit, Department of Autoimmune and Systemic Diseases, Hospital Clinic, University of Barcelona, Centre de Recerca Biomèdica Cellex (IDIBAPS), Barcelona, Spain.
Santos CastañedaDepartment of Rheumatology, Hospital de la Princesa, IIS-Princesa, Madrid, Spain.
Marc RamentolDepartment of Internal Medicine, Hospital Vall d'Hebron, Barcelona, Spain.
Luis Rodriguez-RodriguezDepartment of Rheumatology, Hospital Clínico San Carlos, Madrid, Spain.
Javier NarváezDepartment of Rheumatology, Hospital Universitario de Bellvitge-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain.
Ricardo BlancoDepartment of Rheumatology, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander, Spain.
Norberto Ortego-CentenoSystemic Autoimmune Diseases Unit, Hospital Clínico San Cecilio, Granada, Spain.
Spanish GCA Consortium
Oyvind PalmDepartment of Rheumatology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Andreas P DiamantopoulosDepartment of Rheumatology, Hospital of Southern Norway Trust, Kristiansand, Norway.
Niko BraunDepartment of Internal Medicine, Division of Nephrology, Robert-Bosch-Hospital, Stuttgart, Germany.
Frank MoosigDepartment of Clinical Immunology and Rheumatology, University of Luebeck, Bad Bramstedt, Germany.
Torsten WitteHannover Medical School, Hannover, Germany.
Lorenzo BerettaReferral Center for Systemic Autoimmune Diseases, Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy.
Claudio LunardiDepartment of Medicine, Università degli Studi di Verona, Verona, Italy.
Marco A CimminoDepartment of Internal Medicine, Academic Unit of Clinical Rheumatology, University of Genova, Genova, Italy.
Augusto VaglioDepartment of Clinical Medicine, Nephrology and Health Sciences, University Hospital of Parma, Parma, Italy.
Carlo SalvaraniUnità Operativa di Reumatologia, Azienda Ospedaliera ASMN, Istituto di Ricovero e Cura a Carattere Scientifico, Reggio Emilia, Italy.
Miguel A González-GayDepartment of Rheumatology, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander, Spain.
Javier MartínInstituto de Parasitología y Biomedicina López-Neyra, CSIC, Granada, Spain.
Fundación Marques de Valdecilla · ESInstituto de Investigación Biosanitaria de Granada · ESUniversitat de Barcelona · ESVall d'Hebron Hospital Universitari · ESFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITHNO Bad Bramstedt · DEHospital Clínico San Carlos · ESHospital of Southern Norway · NOHospital Universitario de La Princesa · ESInstitut d'Investigació Biomédica de Bellvitge · ESInstituto de Parasitología y Biomedicina "López - Neyra" · ESMedizinische Hochschule Hannover · DEOslo University Hospital · NORobert Bosch Hospital · DEUniversity of Genoa · ITUniversity of Parma · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIncreased expression of IL-33 and its receptor ST2, encoded by the IL1RL1 gene, has been detected in the inflamed arteries of giant cell arteritis (GCA) patients. The aim of the present study was to investigate for the first time the potential influence of the IL33 and IL1RL1 loci on GCA predisposition.

methodsA total of 1,363 biopsy-proven GCA patients and 3,908 healthy controls from four European cohorts (Spain, Italy, Germany and Norway) were combined in a meta-analysis. Six genetic variants: rs3939286, rs7025417 and rs7044343, within the IL33 gene, and rs2058660, rs2310173 and rs13015714, within the IL1RL1 gene, previously associated with immune-related diseases, were genotyped using predesigned TaqMan assays.

resultsA consistent association between the rs7025417 polymorphism and GCA was evident in the overall meta-analysis, under both allele (P(MH) = 0.041, OR = 0.88, CI 95% 0.78-0.99) and recessive (P(MH) = 3.40E-03, OR = 0.53, CI 95% 0.35-0.80) models. No statistically significant differences between allele or genotype frequencies for the other IL33 and IL1RL1 genetic variants were detected in this pooled analysis.

conclusionsOur results clearly evidenced the implication of the IL33 rs7025417 polymorphism in the genetic network underlying GCA.

Indexed as

AllelesCase-Control StudiesCohort StudiesDisease SusceptibilityFemaleGene Regulatory NetworksGenetic LociGenotypeGiant Cell ArteritisHumansInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MaleOdds RatioPolymorphism, Single NucleotideReceptors, Cell SurfaceIL1RL1 protein, humanInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Receptors, Cell Surface

Identifiers

PMID25409453
PMCPMC4237421
OpenAlexW2017291960

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.