Evidence map›Paper›PMID 40259340›Full record

ArticleBMC rheumatology2025

Transitional and CD21

Sarah McGrath, Boel Sundbeck, Katrin Thorarinsdottir, Charlotte A Jonsson, Alessandro Camponeschi, Monica Leu Agelii, Anna-Karin H Ekwall, Merete Lund Hetland, Mikkel Østergaard, Till Uhlig and 10 more

Abstract read
In one paragraph

Article in BMC rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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.

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

2 citing papers in PubMed.

  1. Review
  2. 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

20 authors.

Sarah McGrath *Department of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Boel Sundbeck *Department of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden. boel.sundbeck@gu.se.
Katrin ThorarinsdottirCenter for Rheumatology Research, Department of Rheumatology, Landspitali University Hospital, Reykjavik, Iceland.
Charlotte A JonssonDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Alessandro CamponeschiDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Monica Leu AgeliiDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Anna-Karin H EkwallDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Merete Lund HetlandCopenhagen Center for Arthritis Research (COPECARE), Center for Rheumatology and Spine Diseases, Centre for Head and Orthopaedics, Rigshospitalet, Glostrup, Copenhagen, Denmark.
Mikkel ØstergaardCopenhagen Center for Arthritis Research (COPECARE), Center for Rheumatology and Spine Diseases, Centre for Head and Orthopaedics, Rigshospitalet, Glostrup, Copenhagen, Denmark.
Till UhligDivision of Rheumatology and Research, Diakonhjemmet Hospital, Oslo, Norway.
Michael NurmohamedDepartment of Rheumatology and Clinical Immunology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Jon LampaDivision of Rheumatology, Department of Medicine, Center for Molecular Medicine (CMM), Karolinska Institute, Stockholm, Sweden.
Dan NordströmDivision of Medicine and Rheumatology, Helsinki University Hospital, Helsinki, Finland.
Kim Hørslev-PetersenDanish Hospital for Rheumatic Diseases, University Hospital of Southern Denmark, Sønderborg, Denmark.
Bjorn GudbjornssonCenter for Rheumatology Research, Department of Rheumatology, Landspitali University Hospital, Reykjavik, Iceland.
Gerdur GröndalCenter for Rheumatology Research, Department of Rheumatology, Landspitali University Hospital, Reykjavik, Iceland.
Ronald van VollenhovenDepartment of Rheumatology and Clinical Immunology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Anna RudinDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Inga-Lill MårtenssonDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
Inger GjertssonDepartment of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEarly initiation of effective treatment is associated with positive long-term prognosis for patients with rheumatoid arthritis (RA). Currently, there are no biomarkers in clinical use to predict treatment response. A predictor of treatment response may be the B-cell compartment, as this is altered in RA patients, making it a potential candidate for predicting treatment response. In this study, we sought to identify B-cell subset(s) at diagnosis that might be associated with Clinical Disease Activity Index (CDAI) remission at 24-week follow-up.

methodsSeventy early RA patients from the NORD-STAR trial, recruited from two Swedish sites, and 28 matched healthy controls, were included in this spin-off study. In NORD-STAR, all patients were randomized to methotrexate (MTX) combined with 1) prednisolone, 2) anti-TNF (certolizumab-pegol), 3) CTLA4-Ig (abatacept), or 4) anti-IL-6R (tocilizumab). Circulating B-cell subsets at diagnosis were assessed by flow cytometry. The primary outcome measure was remission according to CDAI ≤ 2.8. A multivariate two-part discriminant analysis was performed to assess whether B-cell subpopulations at diagnosis could predict remission at 24 weeks. Subsequent univariable statistical analyses were performed using t-tests, Mann-Whitney U, or Kruskal-Wallis tests, as appropriate. Correlations were analyzed using Spearman or Pearson tests, depending on data type. The impact of specific B-cell populations on remission at week 24 was assessed using logistic regression models. The logistic regression model was also used to simultaneously visualize the sensitivity and specificity of the model for all possible values of the exposure (B-cell subpopulations) in predicting the outcome.

resultsPatients who achieved CDAI remission at 24 weeks had higher proportions of transitional (p < 0.01) and CD21

conclusionsOur results indicate that transitional and CD21 CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

B cellEarly rheumatoid arthritisPD-1RemissionRheumatoid arthritisTransitional B cell

Identifiers

PMID40259340
PMCPMC12010607

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.