Evidence map›Paper›PMID 32594150›Full record

ArticleRheumatology (Oxford, England)2020

TLR1/2 and 5 induce elevated cytokine levels from rheumatoid arthritis monocytes independent of ACPA or RF autoantibody status.

Ryan S Thwaites, Sarah Unterberger, Giselle Chamberlain, Karen Walker-Bone, Kevin A Davies, Sandra Sacre

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 14 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

6 authors at 1 institution in 1 country.

Ryan S ThwaitesBrighton and Sussex Medical School, University of Sussex, Brighton, UK.
Sarah UnterbergerBrighton and Sussex Medical School, University of Sussex, Brighton, UK.
Giselle ChamberlainBrighton and Sussex Medical School, University of Sussex, Brighton, UK.
Karen Walker-BoneBrighton and Sussex Medical School, University of Sussex, Brighton, UK.
Kevin A DaviesBrighton and Sussex Medical School, University of Sussex, Brighton, UK.
Sandra SacreBrighton and Sussex Medical School, University of Sussex, Brighton, UK.
Brighton and Sussex Medical School · GB

Funding

Medical Research Council G1001715Medical Research Council MC_U147585823Medical Research Council MC_UU_12011/5
6 · The paper itself

Abstract

objectiveRA is an autoimmune inflammatory joint disease. Both RF and ACPA are associated with more progressive disease and higher levels of systemic inflammation. Monocyte activation of toll-like receptors (TLRs) by endogenous ligands is a potential source of increased production of systemic cytokines. RA monocytes have elevated TLRs, some of which are associated with the disease activity score using 28 joints (DAS28). The aim of this study was to measure TLR-induced cytokine production from monocytes, stratified by autoantibody status, to assess if their capacity to induce cytokines is related to autoantibody status or DAS28.

methodsPeripheral blood monocytes isolated from RA patients and healthy controls were stimulated with TLR1/2, TLR2/6, TLR4, TLR5, TLR7, TLR8 and TLR9 ligands for 18 h before measuring IL-6, TNFα and IL-10. Serum was used to confirm the autoantibody status. Cytokine levels were compared with RF, ACPA and DAS28.

resultsRA monocytes demonstrated significantly increased IL-6 and TNFα upon TLR1/2 stimulation and IL-6 and IL-10 upon TLR5 activation. TLR7 and TLR9 activation did not induce cytokines and no significant differences were observed between RA and healthy control monocytes upon TLR2/6, TLR4 or TLR8 activation. When stratified by ACPA or RF status there were no correlations between autoantibody status and elevated cytokine levels. However, TLR1/2-induced IL-6 did correlate with DAS28.

conclusionsElevated TLR-induced cytokines in RA monocytes were not related to ACPA or RF status. However, TLR1/2-induced IL-6 was associated with disease activity.

Indexed as

AdultAgedAged, 80 and overAnti-Citrullinated Protein AntibodiesAntirheumatic AgentsArthritis, RheumatoidCase-Control StudiesCytokinesFemaleHumansInterleukin-10Interleukin-6LigandsMaleMiddle AgedMonocytesAnti-Citrullinated Protein AntibodiesAntirheumatic AgentsCytokinesIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6LigandsRheumatoid FactorTLR1 protein, humanTLR2 protein, humanTLR5 protein, humanTNF protein, humanToll-Like Receptor 1Toll-Like Receptor 2Toll-Like Receptor 5Toll-Like ReceptorsTumor Necrosis Factor-alphaACPADAS28interleukin-10interleukin-6RFrheumatoid arthritisTNFαtoll-like receptor

Identifiers

PMID32594150
PMCPMC7590412
OpenAlexW3027070744

What OpenQuestion holds

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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.