Evidence map›Paper›PMID 37638026›Full record

ArticleFrontiers in immunology2023

Double-negative-2 B cells are the major synovial plasma cell precursor in rheumatoid arthritis.

Elinor Wing, Catherine Sutherland, Katherine Miles, David Gray, Carl S Goodyear, Thomas D Otto, Stefan Breusch, Graeme Cowan, Mohini Gray

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 34 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Elinor WingCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Catherine SutherlandInstitute of Immunology and Infection Research, School of Biological Sciences, The King's Buildings, The University of Edinburgh, Edinburgh, United Kingdom.
Katherine MilesCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
David GrayInstitute of Immunology and Infection Research, School of Biological Sciences, The King's Buildings, The University of Edinburgh, Edinburgh, United Kingdom.
Carl S GoodyearInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Thomas D OttoInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Stefan BreuschOrthopaedic Unit, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom.
Graeme CowanInstitute of Immunology and Infection Research, School of Biological Sciences, The King's Buildings, The University of Edinburgh, Edinburgh, United Kingdom.
Mohini GrayCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
University of Edinburgh · GBCentre for Inflammation Research · GBUniversity of Glasgow · GBEdinburgh Royal Infirmary · GB

Funding

Medical Research Council MR/N013166/1Wellcome TrustWellcome Trust 220096/Z/20/Z
6 · The paper itself

Abstract

B cells are key pathogenic drivers of chronic inflammation in rheumatoid arthritis (RA). There is limited understanding of the relationship between synovial B cell subsets and pathogenic antibody secreting cells (ASCs). This knowledge is crucial for the development of more targeted B-cell depleting therapies. While CD11c+ double-negative 2 (DN2) B cells have been suggested as an ASC precursor in lupus, to date there is no proven link between the two subsets in RA. We have used both single-cell gene expression and BCR sequencing to study synovial B cells from patients with established RA, in addition to flow cytometry of circulating B cells. To better understand the differentiation patterns within the diseased tissue, a combination of RNA-based trajectory inference and clonal lineage analysis of BCR relationships were used. Both forms of analysis indicated that DN2 B cells serve as a major precursors to synovial ASCs. This study advances our understanding of B cells in RA and reveals the origin of pathogenic ASCs in the RA synovium. Given the significant role of DN2 B cells as a progenitor to pathogenic B cells in RA, it is important to conduct additional research to investigate the origins of DN2 B cells in RA and explore their potential as therapeutic targets in place of the less specific pan-B cells depletion therapies currently in use.

Indexed as

Arthritis, RheumatoidB-Lymphocyte SubsetsAntibody-Producing CellsB-LymphocytesHumansPlasma Cellsantibody secreting cellsdouble-negative-2 (DN2) B cellsrheumatoid arthritissingle-cell sequencingsynovium

Identifiers

PMID37638026
PMCPMC10450142
OpenAlexW4385765500

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.