Evidence map›Paper›PMID 23288628›Full record

ReviewClinical reviews in allergy & immunology2013

Genetics of rheumatoid arthritis - a comprehensive review.

Júlia Kurkó, Timea Besenyei, Judit Laki, Tibor T Glant, Katalin Mikecz, Zoltán Szekanecz

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06459453 (Effects of Kaltenborn Versus Mulligan Techniques on Pain, Range of Motion and Functional Disability in Patients With Rheumatoid Arthritis Of The Wrist.), which is not on this map. Cited by 148 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 10 pooled it
–field-weighted citation impact
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.

NCT06459453 naunknown statusnot on this mapstarted 2023, after this paper: background citation

Effects of Kaltenborn Versus Mulligan Techniques on Pain, Range of Motion and Functional Disability in Patients With Rheumatoid Arthritis Of The Wrist.

TypeinterventionalSponsorRiphah International UniversityRan2023 to 2024Enrolled34ConditionsRheumatoid ArthritisArmsKaltenborn, Mulligan
3 · Its place in the literature

Who cites it

148 citing papers in PubMed, 10 syntheses or guidelines pooled it.

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  11. Long-Term Risk of Rheumatoid Arthritis in Individuals With Autism Spectrum Disorder: A Population-Based Matched Cohort Study.Autism research : official journal of the International Society for Autism Research · 2026
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88 more citing papers are in PubMed but not listed here.

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

6 authors.

Júlia KurkóDepartment of Rheumatology, Institute of Medicine, University of Debrecen Medical and Health Science Center, Nagyerdei str 98, Debrecen, 4032, Hungary.
Timea Besenyei
Judit Laki
Tibor T Glant
Katalin Mikecz
Zoltán Szekanecz

Funding

Mapping of Arthritis Susceptibility GenesR01AR059356 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI GLANT, TIBOR T. · 2010 to 2014
$2.2M
NIAMS NIH HHS R01 AR059356
6 · The paper itself

Abstract

The "Bermuda triangle" of genetics, environment and autoimmunity is involved in the pathogenesis of rheumatoid arthritis (RA). Various aspects of genetic contribution to the etiology, pathogenesis and outcome of RA are discussed in this review. The heritability of RA has been estimated to be about 60 %, while the contribution of HLA to heritability has been estimated to be 11-37 %. Apart from known shared epitope (SE) alleles, such as HLA-DRB1*01 and DRB1*04, other HLA alleles, such as HLA-DRB1*13 and DRB1*15 have been linked to RA susceptibility. A novel SE classification divides SE alleles into S1, S2, S3P and S3D groups, where primarily S2 and S3P groups have been associated with predisposition to seropositive RA. The most relevant non-HLA gene single nucleotide polymorphisms (SNPs) associated with RA include PTPN22, IL23R, TRAF1, CTLA4, IRF5, STAT4, CCR6, PADI4. Large genome-wide association studies (GWAS) have identified more than 30 loci involved in RA pathogenesis. HLA and some non-HLA genes may differentiate between anti-citrullinated protein antibody (ACPA) seropositive and seronegative RA. Genetic susceptibility has also been associated with environmental factors, primarily smoking. Some GWAS studies carried out in rodent models of arthritis have confirmed the role of human genes. For example, in the collagen-induced (CIA) and proteoglycan-induced arthritis (PgIA) models, two important loci - Pgia26/Cia5 and Pgia2/Cia2/Cia3, corresponding the human PTPN22/CD2 and TRAF1/C5 loci, respectively - have been identified. Finally, pharmacogenomics identified SNPs or multiple genetic signatures that may be associated with responses to traditional disease-modifying drugs and biologics.

Indexed as

AnimalsArthritis, RheumatoidDisease Models, AnimalGene-Environment InteractionGenetic Predisposition to DiseaseGenome-Wide Association StudyHLA AntigensHumansMicePolymorphism, GeneticProtein Tyrosine Phosphatase, Non-Receptor Type 22RatsReceptors, InterleukinSmokingTNF Receptor-Associated Factor 1HLA AntigensIL23R protein, humanProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanReceptors, InterleukinTNF Receptor-Associated Factor 1

Identifiers

PMID23288628
PMCPMC3655138

What OpenQuestion holds

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Registered trials

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.