Evidence map›Paper›PMID 27974851›Full record

ReviewNature reviews. Rheumatology2017

Mechanisms leading from systemic autoimmunity to joint-specific disease in rheumatoid arthritis.

Anca I Catrina, Camilla I Svensson, Vivianne Malmström, Georg Schett, Lars Klareskog

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
28.1field-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

116 citing papers in PubMed, 268 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Journal of oral microbiology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

56 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

5 authors at 3 institutions in 2 countries.

Anca I CatrinaRheumatology Unit, Department of Medicine (Solna), Karolinska Institute and Karolinska University Hospital, 171 76 Stockholm, Sweden.
Camilla I SvenssonMolecular Pain Research Group, Department of Physiology and Pharmacology, Karolinska Institute, von Eulers väg 8, 171 65 Stockholm, Sweden.
Vivianne MalmströmRheumatology Unit, Department of Medicine (Solna), Karolinska Institute and Karolinska University Hospital, 171 76 Stockholm, Sweden.
Georg SchettDepartment of Internal Medicine 3, Rheumatology and Immunology, University of Erlangen-Nuremberg, Ulmenweg 18, 91054 Erlangen, Germany.
Lars KlareskogRheumatology Unit, Department of Medicine (Solna), Karolinska Institute and Karolinska University Hospital, 171 76 Stockholm, Sweden.
Karolinska Institutet · SEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A key unanswered question in the pathophysiology of rheumatoid arthritis (RA) is how systemic autoimmunity progresses to joint-specific inflammation. In patients with seropositive RA (that is, characterized by the presence of autoantibodies) evidence is accumulating that immunity against post-translationally modified (such as citrullinated) autoantigens might be triggered in mucosal organs, such as the lung, long before the first signs of inflammation are seen in the joints. However, the mechanism by which systemic autoimmunity specifically homes to the joint and bone compartment, thereby triggering inflammation, remains elusive. This Review summarizes potential pathways involved in this joint-homing mechanism, focusing particularly on osteoclasts as the primary targets of anti-citrullinated protein antibodies (ACPAs) in the bone and joint compartment. Osteoclasts are dependent on citrullinating enzymes for their normal differentiation and are unique in displaying citrullinated antigens on their cell surface in a non-inflamed state. The binding of ACPAs to osteoclasts releases the chemokine IL-8, leading to bone erosion and pain. This process initiates a chain of events that could lead to attraction and activation of neutrophils, resulting in a complex series of proinflammatory processes in the synovium, eventually leading to RA.

Indexed as

Arthritis, RheumatoidAutoantibodiesAutoimmunityBone and BonesHumansJointsOsteoclastsAutoantibodies

Identifiers

PMID27974851
OpenAlexW2560882502

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.