Evidence map›Paper›PMID 28451788›Full record

ReviewSeminars in immunopathology2017

The role of autoantibodies in the pathophysiology of rheumatoid arthritis.

V F A M Derksen, T W J Huizinga, D van der Woude

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in immunopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 7 pooled it
17.9field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 7 syntheses or guidelines pooled it, 313 citations in OpenAlex.

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  17. Correlation between double-stranded DNA and rheumatoid arthritis.Central-European journal of immunology · 2026
    Article
  18. Journal of oral microbiology · 2026
    Review
  19. Article
  20. Article

89 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

3 authors at 1 institution in 1 country.

V F A M DerksenDepartment of Rheumatology, Leiden University Medical Center, C1-R-041, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, the Netherlands.
T W J HuizingaDepartment of Rheumatology, Leiden University Medical Center, C1-R-041, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, the Netherlands. T.J.W.Huizinga@lumc.nl.
D van der WoudeDepartment of Rheumatology, Leiden University Medical Center, C1-R-041, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, the Netherlands.
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint inflammation. The presence of autoantibodies in the sera of RA patients has provided many clues to the underlying disease pathophysiology. Based on the presence of several autoantibodies like rheumatoid factor (RF), anti-citrullinated protein antibodies (ACPA), anti-carbamylated protein antibodies (anti-CarP), and more recently anti-acetylated protein antibodies RA can be subdivided into seropositive and seronegative disease. The formation of these autoantibodies is associated with both genetic and environmental risk factors for RA, like specific human leukocyte antigen (HLA) alleles and smoking. Autoantibodies can be detected many years before disease onset in a subset of patients, suggesting a sequence of events in which the first autoantibodies develop in predisposed hosts, before an inflammatory response ensues leading to clinically apparent arthritis. Research on the characteristics and effector functions of these autoantibodies might provide more insight in pathophysiological processes underlying arthritis in RA. Recent data suggests that ACPA might play a role in perpetuating inflammation once it has developed. Furthermore, pathophysiological mechanisms have been discovered supporting a direct link between the presence of ACPA and both bone erosions and pain in RA patients. In conclusion, investigating the possible pathogenic potential of autoantibodies might lead to improved understanding of the underlying pathophysiological processes in rheumatoid arthritis.

Indexed as

AutoimmunityAnimalsArthritis, RheumatoidAutoantibodiesAutoantigensEnvironmentGene-Environment InteractionGenetic Predisposition to DiseaseHumansMicrobiotaRisk FactorsSignal TransductionAutoantibodiesAutoantigensACPAAutoantibodiesPathophysiologyRheumatoid arthritis

Identifiers

PMID28451788
PMCPMC5486798
OpenAlexW2610107585

What OpenQuestion holds

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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.