Evidence map›Paper›PMID 29895567›Full record

ArticleAnnals of the rheumatic diseases2018

Number of individual ACPA reactivities in synovial fluid immune complexes, but not serum anti-CCP2 levels, associate with inflammation and joint destruction in rheumatoid arthritis.

Azita Sohrabian, Linda Mathsson-Alm, Monika Hansson, Ann Knight, Jörgen Lysholm, Martin Cornillet, Karl Skriner, Guy Serre, Anders Larsson, Tomas Weitoft and 1 more

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Annals of the rheumatic diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  3. Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

11 authors at 7 institutions in 3 countries.

Azita SohrabianDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Linda Mathsson-AlmDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Monika HanssonDepartment of Medicine, Rheumatology Unit, Karolinska Institutet, Stockholm, Sweden.
Ann KnightSection of Rheumatology, Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden.
Jörgen LysholmClinic of Rheumatology, Falu Hospital, Falun, Sweden.
Martin CornilletLaboratory of Epithelial Differentiation and Rheumatoid Autoimmunity, U1056 Inserm, Toulouse University, Toulouse, France.
Karl SkrinerDepartment of Medicine, Charité University Hospital, Berlin, Germany.
Guy SerreLaboratory of Epithelial Differentiation and Rheumatoid Autoimmunity, U1056 Inserm, Toulouse University, Toulouse, France.
Anders LarssonDepartment of Medical Sciences, Section of Clinical Chemistry, Uppsala University, Uppsala, Sweden.
Tomas Weitoft *Department of Research and Development, Section of Rheumatology, Uppsala University/Region of Gävleborg, Gävle, Sweden.
Johan Rönnelid *Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Uppsala University · SEInserm · FRCharité - Universitätsmedizin Berlin · DEFalun Hospital · SEKarolinska Institutet · SEUniversity of Gävle · SEUppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIndividual patients with rheumatoid arthritis (RA) show divergent specific anti-citrullinated protein/peptide antibodies (ACPA) patterns, but hitherto no individual ACPA specificity has consistently been linked to RA pathogenesis. ACPA are also implicated in immune complexes (IC)-associated joint pathology, but until now, there has been no method to investigate the role of individual ACPA in RA IC formation and IC-associated pathogenesis.

methodsWe have developed a new technique based on IC binding to C1q-coated magnetic beads to purify and solubilise circulating IC in sera and synovial fluids (SF) from 77 patients with RA. This was combined with measurement of 19 individual ACPA in serum, SF and in the IC fractions from serum and SF. We investigated whether occurrence of individual ACPA as well as number of ACPA in these compartments was related to clinical and laboratory measures of disease activity and inflammation.

resultsThe majority of individual ACPA reactivities were enriched in SF as compared with in serum, and levels of ACPA in IC were regulated independently of levels in serum and SF. No individual ACPA reactivity in any compartment showed a dominating association to clinical and laboratory measures of disease activity and severity. Instead, the number of individual ACPA reactivities in the IC fraction from SF associated with a number of markers of joint destruction and inflammation.

conclusionsOur data highlight the polyclonality of ACPA in joint IC and the possibility that a broad ACPA repertoire in synovial fluid IC might drive the local inflammatory and matrix-degrading processes in joints, in analogy with antibody-induced rodent arthritis models.

Indexed as

AdultAgedAntibody SpecificityAnti-Citrullinated Protein AntibodiesAntigen-Antibody ComplexArthritis, RheumatoidCase-Control StudiesFemaleHumansMaleMicroarray AnalysisMiddle AgedSeverity of Illness IndexSynovial FluidAnti-Citrullinated Protein AntibodiesAntigen-Antibody Complexant-ccpautoantibodiesrheumatoid arthritissynovial fluid

Identifiers

PMID29895567
PMCPMC6104681
OpenAlexW2808487458

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.