Evidence map›Paper›PMID 16846531›Full record

ArticleArthritis research & therapy2006

Coexpression and interaction of CXCL10 and CD26 in mesenchymal cells by synergising inflammatory cytokines: CXCL8 and CXCL10 are discriminative markers for autoimmune arthropathies.

Paul Proost, Sofie Struyf, Tamara Loos, Mieke Gouwy, Evemie Schutyser, René Conings, Isabelle Ronsse, Marc Parmentier, Bernard Grillet, Ghislain Opdenakker and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Arthritis research & therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 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

12 authors at 4 institutions in 2 countries.

Paul ProostLaboratory of Molecular Immunology, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium. paul.proost@rega.kuleuven.be
Sofie Struyf
Tamara Loos
Mieke Gouwy
Evemie Schutyser
René Conings
Isabelle Ronsse
Marc Parmentier
Bernard Grillet
Ghislain Opdenakker
Jan Balzarini
Jo Van Damme
Rega Institute for Medical Research · BEKU Leuven · BEDow Chemical (Netherlands) · NLUniversité Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukocyte infiltration during acute and chronic inflammation is regulated by exogenous and endogenous factors, including cytokines, chemokines and proteases. Stimulation of fibroblasts and human microvascular endothelial cells with the inflammatory cytokines interleukin-1beta (IL-1beta) or tumour necrosis factor alpha (TNF-alpha) combined with either interferon-alpha (IFN-alpha), IFN-beta or IFN-gamma resulted in a synergistic induction of the CXC chemokine CXCL10, but not of the neutrophil chemoattractant CXCL8. In contrast, simultaneous stimulation with different IFN types did not result in a synergistic CXCL10 protein induction. Purification of natural CXCL10 from the conditioned medium of fibroblasts led to the isolation of CD26/dipeptidyl peptidase IV-processed CXCL10 missing two NH2-terminal residues. In contrast to intact CXCL10, NH2-terminally truncated CXCL10(3-77) did not induce extracellular signal-regulated kinase 1/2 or Akt/protein kinase B phosphorylation in CXC chemokine receptor 3-transfected cells. Together with the expression of CXCL10, the expression of membrane-bound CD26/dipeptidyl peptidase IV was also upregulated in fibroblasts by IFN-gamma, by IFN-gamma plus IL-1beta or by IFN-gamma plus TNF-alpha. This provides a negative feedback for CXCL10-dependent chemotaxis of activated T cells and natural killer cells. Since TNF-alpha and IL-1beta are implicated in arthritis, synovial concentrations of CXCL8 and CXCL10 were compared in patients suffering from crystal arthritis, ankylosing spondylitis, psoriatic arthritis and rheumatoid arthritis. All three groups of autoimmune arthritis patients (ankylosing spondylitis, psoriatic arthritis and rheumatoid arthritis) had significantly increased synovial CXCL10 levels compared with crystal arthritis patients. In contrast, compared with crystal arthritis, only rheumatoid arthritis patients, and not ankylosing spondylitis or psoriatic arthritis patients, had significantly higher synovial CXCL8 concentrations. Synovial concentrations of the neutrophil chemoattractant CXCL8 may therefore be useful to discriminate between autoimmune arthritis types.

Indexed as

Autoimmune DiseasesBiomarkersCells, CulturedChemokine CXCL10Chemokines, CXCCytokinesDermisDipeptidyl Peptidase 4Drug CombinationsEndothelial CellsFibroblastsHumansInfant, NewbornInflammation MediatorsInterleukin-8Joint DiseasesBiomarkersChemokine CXCL10Chemokines, CXCCXCL10 protein, humanCXCR3 protein, humanCytokinesDipeptidyl Peptidase 4Drug CombinationsInflammation MediatorsInterleukin-8LigandsPeptide FragmentsProtein IsoformsReceptors, ChemokineReceptors, CXCR3

Identifiers

PMID16846531
PMCPMC1779382
OpenAlexW1591498266

What OpenQuestion holds

Textmetadata
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.