Evidence map›Paper›PMID 28847766›Full record

ArticleAnnals of the rheumatic diseases2017

Identification of a transitional fibroblast function in very early rheumatoid arthritis.

Andrew Filer, Lewis S C Ward, Samuel Kemble, Christopher S Davies, Hafsa Munir, Rebekah Rogers, Karim Raza, Christopher Dominic Buckley, Gerard B Nash, Helen M McGettrick

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 66 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

10 authors at 3 institutions in 1 country.

Andrew FilerRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Lewis S C WardRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Samuel KembleRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Christopher S DaviesUniversity Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
Hafsa MunirInstitute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK.
Rebekah RogersRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Karim RazaRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Christopher Dominic BuckleyRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Gerard B NashInstitute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK.
Helen M McGettrickRheumatology Research Group, Arthritis Research UK Centre of Excellence in the Pathogenesis of Rheumatoid Arthritis, Institute of Inflammation and Ageing, Birmingham, UK.
Sandwell & West Birmingham Hospitals NHS Trust · GBUniversity of Birmingham · GBUniversity Hospitals Birmingham NHS Foundation Trust · GB

Funding

British Heart Foundation PG/14/28/30774Versus Arthritis 19791Versus Arthritis 19899Wellcome Trust
6 · The paper itself

Abstract

objectivesSynovial fibroblasts actively regulate the inflammatory infiltrate by communicating with neighbouring endothelial cells (EC). Surprisingly, little is known about how the development of rheumatoid arthritis (RA) alters these immunomodulatory properties. We examined the effects of phase of RA and disease outcome (resolving vs persistence) on fibroblast crosstalk with EC and regulation of lymphocyte recruitment.

methodsFibroblasts were isolated from patients without synovitis, with resolving arthritis, very early RA (VeRA; symptom ≤12 weeks) and established RA undergoing joint replacement (JRep) surgery. Endothelial-fibroblast cocultures were formed on opposite sides of porous filters. Lymphocyte adhesion from flow, secretion of soluble mediators and interleukin 6 (IL-6) signalling were assessed.

resultsFibroblasts from non-inflamed and resolving arthritis were immunosuppressive, inhibiting lymphocyte recruitment to cytokine-treated endothelium. This effect was lost very early in the development of RA, such that fibroblasts no longer suppressed recruitment. Changes in IL-6 and transforming growth factor beta 1 (TGF-β

conclusionsIn RA, fibroblasts undergo two distinct changes in function: first a loss of immunosuppressive responses early in disease development, followed by the later acquisition of a stimulatory phenotype. Fibroblasts exhibit a transitional functional phenotype during the first 3 months of symptoms that contributes to the accumulation of persistent infiltrates. Finally, the role of IL-6 and TGF-β

Indexed as

AdultArthritis, RheumatoidCoculture TechniquesCytokinesEpithelial CellsFemaleFibroblastsHumansInterleukin-6LymphocytesMaleMiddle AgedSynovial MembraneTransforming Growth Factor beta1CytokinesIL6 protein, humanInterleukin-6Transforming Growth Factor beta1adhesionendothelial cellsFibroblastslymphocytesrheumatoid arthritis

Identifiers

PMID28847766
PMCPMC5705853
OpenAlexW2746181579

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.