Evidence map›Paper›PMID 29959183›Full record

ArticleAnnals of the rheumatic diseases2018

Non-classical monocytes as mediators of tissue destruction in arthritis.

Antonia Puchner, Victoria Saferding, Michael Bonelli, Yohei Mikami, Melanie Hofmann, Julia S Brunner, Michael Caldera, Eliana Goncalves-Alves, Nikolaus B Binder, Anita Fischer and 13 more

Abstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
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

49 citing papers in PubMed.

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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

23 authors.

Antonia PuchnerDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Victoria SaferdingDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Michael BonelliDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Yohei MikamiMolecular Immunology and Inflammation Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA.
Melanie HofmannDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Julia S BrunnerDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Michael CalderaCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Eliana Goncalves-AlvesDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Nikolaus B BinderDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Anita FischerDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Elisabeth SimaderDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Carl-Walter SteinerDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Harald LeissDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Silvia HayerDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Birgit NiederreiterDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Thomas KaronitschDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Marije I KoendersDepartment of Experimental Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands.
Bruno K PodesserDepartment of Biomedical Research, Medical University of Vienna, Vienna, Austria.
John J O'SheaMolecular Immunology and Inflammation Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA.
Jörg MencheCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Josef S SmolenDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Kurt RedlichDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Stephan BlümlDivision of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Funding

Stat transcription factors in immunoregulation and autoimmune diseaseZIAAR041159 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2025
$49.3M
High Throughput Next Generation Sequencing: supports genomics and epigenomics research in muscle, skin, bone and autoimmune diseases.ZICAR041207 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI DELL'ORSO, STEFANIA · 2016 to 2025
$12.3M
6 · The paper itself

Abstract

objectivesBone destruction in rheumatoid arthritis is mediated by osteoclasts (OC), which are derived from precursor cells of the myeloid lineage. The role of the two monocyte subsets, classical monocytes (expressing CD115, Ly6C and CCR2) and non-classical monocytes (which are CD115 positive, but low in Ly6C and CCR2), in serving as precursors for OC in arthritis is still elusive.

methodsWe investigated CCR2

resultsWe show that in hTNFtg arthritis local bone erosion and OC generation are even enhanced in the absence of CCR2. We further show the numbers of non-classical monocytes in blood are elevated and are significantly correlated with histological signs of joint destruction. Sorted non-classical monocytes display an increased capacity to differentiate into OCs. This is associated with an increased expression of signal transduction components of RANK, most importantly TRAF6, leading to an increased responsiveness to RANKL.

conclusionTherefore, non-classical monocytes are pivotal cells in arthritis tissue damage and a possible target for therapeutically intervention for the prevention of inflammatory joint damage.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidBone ResorptionCell DifferentiationDisease Models, AnimalFlow CytometryMiceMonocytesOsteoclastsRANK LigandReceptor Activator of Nuclear Factor-kappa BReceptors, CCR2Signal TransductionTNF Receptor-Associated Factor 6Ccr2 protein, mouseRANK LigandReceptor Activator of Nuclear Factor-kappa BReceptors, CCR2TNF Receptor-Associated Factor 6Tnfrsf11a protein, mouseTnfsf11 protein, mouseTRAF6 protein, mousearthritiscytokinesinflammationsynovitistnf-alpha

Identifiers

PMID29959183
PMCPMC6161666

What OpenQuestion holds

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Registered trials

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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.