Evidence map›Paper›PMID 15140777›Full record

ArticleAnnals of the rheumatic diseases2004

High production of proinflammatory and Th1 cytokines by dendritic cells from patients with rheumatoid arthritis, and down regulation upon FcgammaR triggering.

T R D J Radstake, P L E M van Lent, G J Pesman, A B Blom, F G J Sweep, J Rönnelid, G J Adema, P Barrera, W B van den Berg

Open access · bronzeAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Review
  3. Future therapeutic targets in rheumatoid arthritis?Seminars in immunopathology · 2017
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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 3 institutions in 2 countries.

T R D J RadstakeDepartment of Experimental Rheumatology, University Medical Centre, Nijmegen, The Netherlands. T.Radstake@reuma.umcn.nl
P L E M van Lent
G J Pesman
A B Blom
F G J Sweep
J Rönnelid
G J Adema
P Barrera
W B van den Berg
Radboud University Nijmegen · NLRadboud University Medical Center · NLUppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo assess whether DC from RA produce altered cytokine levels and whether this is regulated by triggering of Fc gamma receptors (FcgammaR).

methodsThe production of proinflammatory (TNFalpha, IL1, IL6), Th1 (IL12, IFNgamma), and Th2 (IL10) cytokine profiles of immature DC (iDC) from patients with RA and healthy subjects upon triggering of FcgammaR dependent and independent pathways was investigated. iDC, derived from blood monocytes by standardised protocols, were stimulated with immune complexes (IC) at day 6 for 48 hours and, subsequently, for 2 days with LPS in the presence or absence of IC or IFNgamma, resulting in fully matured DC (mDC). IL1, IL6, TNFalpha, IFNgamma, IL12, and IL10 levels in supernatants were measured by ELISA and RIA.

resultsmDC from patients with RA showed a markedly increased production of IL1, IL6, TNFalpha, and IL10 compared with DC from healthy donors. Triggering of FcgammaR decreased the production of proinflammatory cytokines IL1, IL12, and IFNgamma by iDC and mDC in RA and controls. The production of IL6 and TNFalpha decreased in patients with RA, whereas it was increased in controls. Triggering of FcgammaR independent mechanisms using IFNgamma increased the production of proinflammatory and Th1 cytokines, which was more pronounced in RA.

conclusionFcgammaR dependent pathways influence cytokine production by DC. A skewed balance towards proinflammatory and Th1 cytokines in RA can, at least partly, be restored by triggering FcgammaR on DC in RA. Insight into the mechanism which determines the FcgammaR balance might lead to new strategies to abrogate Th1 driven inflammatory processes in RA.

Indexed as

Arthritis, RheumatoidCytokinesDendritic CellsDown-RegulationEnzyme-Linked Immunosorbent AssayFlow CytometryHumansInterferon-gammaInterleukinsRadioimmunoassayReceptors, IgGTumor Necrosis Factor-alphaCytokinesInterferon-gammaInterleukinsReceptors, IgGTumor Necrosis Factor-alpha

Identifiers

PMID15140777
PMCPMC1755036
OpenAlexW2119110179

What OpenQuestion holds

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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.