Evidence map›Paper›PMID 16802344›Full record

ArticleArthritis and rheumatism2006

Differential survival of leukocyte subsets mediated by synovial, bone marrow, and skin fibroblasts: site-specific versus activation-dependent survival of T cells and neutrophils.

Andrew Filer, Greg Parsonage, Emily Smith, Chloe Osborne, Andrew M C Thomas, S John Curnow, G Ed Rainger, Karim Raza, Gerard B Nash, Janet Lord and 2 more

Open access · greenAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 101 citations in OpenAlex.

  1. Modulation of TNF-induced macrophage polarization by synovial fibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2014
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  19. Stroma: the forgotten cells of innate immune memory.Clinical and experimental immunology · 2018
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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

12 authors at 3 institutions in 1 country.

Andrew FilerMRC Centre for Immune Regulation, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Greg Parsonage
Emily Smith
Chloe Osborne
Andrew M C Thomas
S John Curnow
G Ed Rainger
Karim Raza
Gerard B Nash
Janet Lord
Mike Salmon
Christopher D Buckley
Immune Regulation (United Kingdom) · GBUniversity of Birmingham · GBRoyal Orthopaedic Hospital · GB

Funding

Arthritis Research UK 16390Medical Research Council G116/131
6 · The paper itself

Abstract

objectiveSynovial fibroblasts share a number of phenotype markers with fibroblasts derived from bone marrow. In this study we investigated the role of matched fibroblasts obtained from 3 different sources (bone marrow, synovium, and skin) to test the hypothesis that synovial fibroblasts share similarities with bone marrow-derived fibroblasts in terms of their ability to support survival of T cells and neutrophils.

methodsMatched synovial, bone marrow, and skin fibroblasts were established from 8 different patients with rheumatoid arthritis who were undergoing knee or hip surgery. Resting or activated fibroblasts were cocultured with either CD4 T cells or neutrophils, and the degree of leukocyte survival, apoptosis, and proliferation were measured.

resultsFibroblasts derived from all 3 sites supported increased survival of CD4 T cells, mediated principally by interferon-beta. However, synovial and bone marrow fibroblasts shared an enhanced site-specific ability to maintain CD4 T cell survival in the absence of proliferation, an effect that was independent of fibroblast activation or proliferation but required direct T cell-fibroblast cell contact. In contrast, fibroblast-mediated neutrophil survival was less efficient, being independent of the site of origin of the fibroblast but dependent on prior fibroblast activation, and mediated solely by soluble factors, principally granulocyte-macrophage colony-stimulating factor.

conclusionThese results suggest an important functional role for fibroblasts in the differential accumulation of leukocyte subsets in a variety of tissue microenvironments. The findings also provide a potential explanation for site-specific differences in the pattern of T cell and neutrophil accumulation observed in chronic inflammatory diseases.

Indexed as

ApoptosisArthritis, RheumatoidBone MarrowCD4-Positive T-LymphocytesCell CommunicationCell ProliferationCell SurvivalCoculture TechniquesCytokinesFibroblastsFibronectinsGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon-betaNeutrophilsCytokinesFibronectinsGranulocyte-Macrophage Colony-Stimulating FactorInterferon-betaTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID16802344
PMCPMC3119431
OpenAlexW2045984032

What OpenQuestion holds

Textmetadata
LicenceTDM
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.