Evidence map›Paper›PMID 26314565›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2016

Phenotypic, Functional, and Gene Expression Profiling of Peripheral CD45RA+ and CD45RO+ CD4+CD25+CD127(low) Treg Cells in Patients With Chronic Rheumatoid Arthritis.

Gina J Walter, Veerle Fleskens, Klaus S Frederiksen, Megha Rajasekhar, Bina Menon, Jens G Gerwien, Hayley G Evans, Leonie S Taams

Open access · hybridAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
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  3. Interleukin-6 (IL-6) Receptor Antagonist Protects Against Rheumatoid Arthritis.Medical science monitor : international medical journal of experimental and clinical research · 2016
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  4. Review
  5. Article
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  12. Article
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  15. Automated clustering reveals CD4Frontiers in immunology · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 2 countries.

Gina J WalterKing's College London, London, UK.
Veerle FleskensKing's College London, London, UK.
Klaus S FrederiksenNovo Nordisk, Måløv, Denmark.
Megha RajasekharKing's College London, London, UK.
Bina MenonGuy's and St. Thomas' NHS Foundation Trust, London, UK.
Jens G GerwienNovo Nordisk, Måløv, Denmark.
Hayley G EvansKing's College London, London, UK.
Leonie S TaamsKing's College London, London, UK.
King's College London · GBNovo Nordisk (Denmark) · DKGuy's and St Thomas' NHS Foundation Trust · GB

Funding

Arthritis Research UK 19307Cancer Research UK 19307Department of Health
6 · The paper itself

Abstract

objectiveConflicting evidence exists regarding the suppressive capacity of Treg cells in the peripheral blood (PB) of patients with rheumatoid arthritis (RA). The aim of this study was to determine whether Treg cells are intrinsically defective in RA.

methodsUsing a range of assays on PB samples from patients with chronic RA and healthy controls, CD3+CD4+CD25+CD127(low) Treg cells from the CD45RO+ or CD45RA+ T cell compartments were analyzed for phenotype, cytokine expression (ex vivo and after in vitro stimulation), suppression of Teff cell proliferation and cytokine production, suppression of monocyte-derived cytokine/chemokine production, and gene expression profiles.

resultsNo differences between RA patients and healthy controls were observed with regard to the frequency of Treg cells, ex vivo phenotype (CD4, CD25, CD127, CD39, or CD161), or proinflammatory cytokine profile (interleukin-17 [IL-17], interferon-γ [IFNγ], or tumor necrosis factor [TNF]). FoxP3 expression was slightly increased in Treg cells from RA patients. The ability of Treg cells to suppress the proliferation of T cells or the production of cytokines (IFNγ or TNF) upon coculture with autologous CD45RO+ Teff cells and monocytes was not significantly different between RA patients and healthy controls. In PB samples from some RA patients, CD45RO+ Treg cells showed an impaired ability to suppress the production of certain cytokines/chemokines (IL-1β, IL-1 receptor antagonist, IL-7, CCL3, or CCL4) by autologous lipopolysaccharide-activated monocytes. However, this was not observed in all patients, and other cytokines/chemokines (TNF, IL-6, IL-8, IL-12, IL-15, or CCL5) were generally suppressed. Finally, gene expression profiling of CD45RA+ or CD45RO+ Treg cells from the PB revealed no statistically significant differences between RA patients and healthy controls.

conclusionOur findings indicate that there is no global defect in either CD45RO+ or CD45RA+ Treg cells in the PB of patients with chronic RA.

Indexed as

AdolescentAdultAgedAged, 80 and overArthritis, RheumatoidCase-Control StudiesCD4 AntigensCytokinesFemaleFlow CytometryGene Expression ProfilingHumansInterferon-gammaInterleukin-10Interleukin-17Interleukin-2 Receptor alpha SubunitCD4 AntigensCytokinesIL10 protein, humanInterferon-gammaInterleukin-10Interleukin-17Interleukin-2 Receptor alpha SubunitInterleukin-7 Receptor alpha SubunitLeukocyte Common AntigensTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID26314565
PMCPMC4832388
OpenAlexW2207804031

What OpenQuestion holds

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LicenceCC BY
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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.