Evidence map›Paper›PMID 23607884›Full record

ArticleClinical and experimental immunology2013

Genetic variants in the region of the C1q genes are associated with rheumatoid arthritis.

L A Trouw, N Daha, F A S Kurreeman, S Böhringer, G N Goulielmos, H J Westra, A Zhernakova, L Franke, E A Stahl, E W N Levarht and 7 more

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Complement C1q expression in Erythema nodosum leprosum.PLoS neglected tropical diseases · 2018
    Article
  11. Article
  12. Article
  13. Arthritis models: usefulness and interpretation.Seminars in immunopathology · 2017
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Autoimmunity in 2013.Clinical reviews in allergy & immunology · 2014
    Review
  20. 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

17 authors at 5 institutions in 3 countries.

L A TrouwDepartment of Rheumatology, Leiden University Medical Center, The Netherlands. L.A.Trouw@lumc.nl
N Daha
F A S Kurreeman
S Böhringer
G N Goulielmos
H J Westra
A Zhernakova
L Franke
E A Stahl
E W N Levarht
G Stoeken-Rijsbergen
W Verduijn
A Roos
Y Li
J J Houwing-Duistermaat
T W J Huizinga
R E M Toes
Leiden University Medical Center · NLBrigham and Women's Hospital · USUniversity Medical Center Groningen · NLUniversity of Crete · GRUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rodent models for arthritis implicate a role for complement in disease development and progression. In humans, complement deposition has been observed in inflamed synovia of rheumatoid arthritis (RA) patients. In this study we analysed whether genetic variants of complement component C1q predispose to RA. We genotyped single nucleotide polymorphisms (SNPs) in and around the C1q genes, C1qA, C1qB and C1qC, in a Dutch set of 845 RA cases and 1046 controls. Replication was sought in a sample set from North America (868 cases/1193 controls), and a meta-analysis was performed in a combined samples set of 8000 cases and 23 262 controls of European descent. We determined C1q serum levels in relation to C1q genotypes. In the discovery phase, five of the 13 SNPs tested in the C1q genes showed a significant association with RA. Additional analysis of the genomic area around the C1q genes revealed that the strongest associating SNPs were confined to the C1q locus. Within the C1q locus we observed no additional signal independent of the strongest associating SNP, rs292001 [odds ratio (OR) = 0·72 (0·58-0·88), P = 0·0006]. The variants of this SNP were associated with different C1q serum levels in healthy controls (P = 0·006). Interestingly, this SNP was also associated significantly in genome-wide association studies (GWAS) from the North American Rheumatoid Arthritis Consortium study, confirming the association with RA [OR = 0·83 (0·69-1·00), P = 0·043]. Combined analysis, including integrated data from six GWAS studies, provides support for the genetic association. Genetic variants in C1q are correlated with C1q levels and may be a risk for the development of RA.

Indexed as

Polymorphism, Single NucleotideArthritis, RheumatoidCanadaCohort StudiesComplement C1qGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeGreeceHumansNetherlandsReceptor, EphA8Receptor, EphB2RNA, MessengerUnited StatesComplement C1qReceptor, EphA8Receptor, EphB2RNA, Messenger

Identifiers

PMID23607884
PMCPMC3694537
OpenAlexW1537575434

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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.