Evidence map›Paper›PMID 20158887›Full record

ArticleArthritis research & therapy2010

Functional consequences of DECTIN-1 early stop codon polymorphism Y238X in rheumatoid arthritis.

Theo S Plantinga, Jaap Fransen, Nozomi Takahashi, Rinke Stienstra, Piet L van Riel, Wim B van den Berg, Mihai G Netea, Leo Ab Joosten

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Dectin-1: a role in antifungal defense and consequences of genetic polymorphisms in humans.Mammalian genome : official journal of the International Mammalian Genome Society · 2011
    Review
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.

Theo S PlantingaDepartment of Medicine, Radboud University Nijmegen Medical Centre, P,O, Box 9101, 6500 HB Nijmegen, The Netherlands. t.plantinga@aig.umcn.nl
Jaap Fransen
Nozomi Takahashi
Rinke Stienstra
Piet L van Riel
Wim B van den Berg
Mihai G Netea
Leo Ab Joosten
Radboud University Nijmegen · NLRadboud University Medical Center · NLVIB-UGent Center for Inflammation Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDectin-1, a pattern recognition receptor expressed by the innate immune system, is known to be a major receptor inducing Th17-type adaptive immune responses that have been demonstrated to mediate autoimmunity. In this study, dectin-1 mRNA and protein expression, as well as the recently characterized DECTIN-1 Y238X early stop codon polymorphism, were studied in relation to rheumatoid arthritis (RA) susceptibility and severity.

methodsDectin-1 mRNA expression was measured in synovial tissue specimens of RA, osteoarthritis (OA), and nonrheumatic patients. Dectin-1 protein expression and localization were assessed in RA synovial tissue specimens. Macrophages from individuals with different DECTIN-1 genotypes were examined for differences in cytokine responses on dectin-1 stimulation. Furthermore, clinical parameters of inflammation and bone destruction of 262 RA patients were correlated with the presence of the DECTIN-1 Y238X polymorphism.

resultsEvaluation of dectin-1 mRNA expression in synovial tissue biopsies revealed an increased expression in RA specimens, compared with biopsies from OA and nonrheumatic patients. Accordingly, dectin-1 protein expression in RA synovial tissue biopsies was moderate to high, especially on macrophage-like cells. Cytokine production capacity of macrophages bearing the DECTIN-1 Y238X polymorphism was demonstrated to be impaired on dectin-1 stimulation. However, the presence of the DECTIN-1 Y238X polymorphism was not associated with RA susceptibility or disease severity.

conclusionsAlthough expression of dectin-1 was high in synovial tissue of RA patients, and reduced cytokine production was observed in macrophages of individuals bearing the DECTIN-1 Y238X polymorphism, loss of one functional allele of DECTIN-1 is not associated with either susceptibility to or severity of RA.

Indexed as

Genetic Predisposition to DiseaseArthritis, RheumatoidCodon, TerminatorDectin-1Enzyme-Linked Immunosorbent AssayGene ExpressionHumansImmunohistochemistryLectins, C-TypeMembrane ProteinsNerve Tissue ProteinsPolymorphism, Single NucleotideReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSynovial MembraneCodon, TerminatorDectin-1Lectins, C-TypeMembrane ProteinsNerve Tissue ProteinsRNA, Messenger

Identifiers

PMID20158887
PMCPMC2875660
OpenAlexW2119472512

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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.