Evidence map›Paper›PMID 28053322›Full record

ArticleGenes and immunity2017

VAV1 regulates experimental autoimmune arthritis and is associated with anti-CCP negative rheumatoid arthritis.

A O Guerreiro-Cacais, U Norin, A Gyllenberg, R Berglund, A D Beyeen, Rheumatoid Arthritis Consortium International (RACI), E Petit-Teixeira, F Cornélis, A Saoudi, G J Fournié and 7 more

Erratum issuedAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. TheJournal of inflammation research · 2023
    Article
  3. CD4Epigenetics · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. International journal of environmental research and public health · 2020
    Article
  9. Article
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 2 countries.

A O Guerreiro-CacaisDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
U NorinDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
A GyllenbergDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
R BerglundDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
A D BeyeenDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Rheumatoid Arthritis Consortium International (RACI)
E Petit-TeixeiraGenHotel-EA3886, Evry-Val d'Essonne University, Evry-Genopole, France.
F CornélisGenHotel-Auvergne, CHU de Clermont-Ferrand, Auvergne University, France.
A SaoudiInserm, U1043, Toulouse, France.
G J FourniéInserm, U1043, Toulouse, France.
R HolmdahlDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
L AlfredssonDepartment of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
L KlareskogRheumatology Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
M JagodicDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
T OlssonDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
I KockumDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
L PadyukovRheumatology Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
Karolinska Institutet · SEInserm · FRKarolinska University Hospital · SEUniversité Clermont Auvergne · FRUniversité d'Évry Val-d'Essonne · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) patients can be stratified into two subgroups defined by the presence or absence of antibodies against citrullinated circular peptides (anti-CCP) with most of the genetic association found in anti-CCP positive RA. Here we addressed the role of VAV1, previously associated to multiple sclerosis (MS), in the pathogenesis of RA in experimental models and in a genetic association study. Experimental arthritis triggered by pristane or collagen type II was induced in DA rats and in the DA.BN-R25 congenic line that carries a polymorphism in Vav1. Difference in arthritis severity was observed only after immunization with pristane. In a case-control study, 34 SNPs from VAV1 locus were analyzed by Immunochip genotyping in 11475 RA patients (7573 anti-CCP positive and 3902 negative) and 15,870 controls in six cohorts of European Caucasians. A combination of the previous MS-associated haplotype and two additional SNPs was associated with anti-CCP negative RA (alleles G-G-A-A of rs682626-rs2546133-rs2617822-rs12979659, OR=1.13, P=1.27 × 10

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidAutoantibodiesAutoimmune DiseasesBiomarkersCase-Control StudiesCohort StudiesFemaleGenetic Predisposition to DiseaseHumansMalePeptides, CyclicPolymorphism, GeneticPrognosisProto-Oncogene Proteins c-vavAutoantibodiesBiomarkerscyclic citrullinated peptidePeptides, CyclicProto-Oncogene Proteins c-vavVAV1 protein, human

Identifiers

PMID28053322
OpenAlexW2568135939

What OpenQuestion holds

Textmetadata
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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.