Evidence map›Paper›PMID 30518680›Full record

ArticleJCI insight2018

Enriched Cd141+ DCs in the joint are transcriptionally distinct, activated, and contribute to joint pathogenesis.

Mary Canavan, Alice M Walsh, Vipul Bhargava, Sarah M Wade, Trudy McGarry, Viviana Marzaioli, Barry Moran, Monika Biniecka, Hannah Convery, Siobhan Wade and 6 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-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

28 citing papers in PubMed, 41 citations in OpenAlex.

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  19. CD209/CD14Frontiers in immunology · 2021
    Article
  20. Functionally Mature CD1cFrontiers in immunology · 2021
    Article
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

16 authors at 4 institutions in 2 countries.

Mary CanavanMolecular Rheumatology, School of Medicine, Trinity College Dublin, Ireland.
Alice M WalshImmunology and.
Vipul BhargavaDiscovery Sciences, Janssen Research & Development, Spring House, Pennsylvania, USA.
Sarah M WadeMolecular Rheumatology, School of Medicine, Trinity College Dublin, Ireland.
Trudy McGarryMolecular Rheumatology, School of Medicine, Trinity College Dublin, Ireland.
Viviana MarzaioliMolecular Rheumatology, School of Medicine, Trinity College Dublin, Ireland.
Barry MoranSchool of Biochemistry and Immunology, Trinity College Dublin, Ireland.
Monika BinieckaCentre for Arthritis & Rheumatic Diseases, St. Vincent's University Hospital, University College Dublin, Ireland.
Hannah ConveryCentre for Arthritis & Rheumatic Diseases, St. Vincent's University Hospital, University College Dublin, Ireland.
Siobhan WadeMolecular Rheumatology, School of Medicine, Trinity College Dublin, Ireland.
Carl OrrCentre for Arthritis & Rheumatic Diseases, St. Vincent's University Hospital, University College Dublin, Ireland.
Ronan MullanDepartment of Rheumatology, Adelaide and Meath Hospital, Dublin, Ireland.
Jean M FletcherTranslational Immunology, Schools of Biochemistry and Immunology and Medicine, Trinity College Dublin, Ireland.
Sunil NagpalImmunology and.
Douglas J VealeCentre for Arthritis & Rheumatic Diseases, St. Vincent's University Hospital, University College Dublin, Ireland.
Ursula FearonMolecular Rheumatology, School of Medicine, Trinity College Dublin, Ireland.
Trinity College Dublin · IESt. Vincent's University Hospital · IESpringhouse · USTallaght University Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD141+ DC are implicated in antiviral and antitumor immunity. However, mechanistic studies in autoimmune disease are limited. This is the first study to our knowledge examining CD141+ DC in autoimmune disease, specifically inflammatory arthritis (IA). We identified significant enrichment of CD141+ DC in the inflamed synovial joint, which were transcriptionally distinct from IA and healthy control (HC) blood CD141+ DC and significantly more activated, and they exhibited increased responsiveness to TLR3. Synovial CD141+ DC represent a bone fide CD141+ DC population that is distinct from CD1c+ DC. Synovial CD141+ DC induced higher levels of CD4+ and CD8+ T cell activation compared with their peripheral blood counterparts, as made evident by expression of IFN-γ, TNF-α, and granulocyte-macrophage CSF (GMCSF). Autologous synovial CD141+ DC cocultures also induce higher levels of these cytokines, further highlighting their contribution to synovial inflammation. Synovial CD141+ DC-T cell interactions had the ability to further activate synovial fibroblasts, inducing adhesive and invasive pathogenic mechanisms. Furthermore, we identify a mechanism in which synovial CD141+ DC are activated, via ligation of the hypoxia-inducible immune-amplification receptor TREM-1, which increased synovial CD141+ DC activation, migratory capacity, and proinflammatory cytokines. Thus, synovial CD141+ DC display unique mechanistic and transcriptomic signatures, which are distinguishable from blood CD141+ DC and can contribute to synovial joint inflammation.

Indexed as

AdultAntigens, CD1Antigens, SurfaceArthritis, RheumatoidAutoimmune DiseasesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDendritic CellsFemaleGlycoproteinsHumansInflammationInterferon-gammaJoint DiseasesLymphocyte ActivationAntigens, CD1Antigens, SurfaceCD1C protein, humanCytokinesGlycoproteinsInterferon-gammaReceptors, ImmunologicTHBD protein, humanThrombomodulinTLR3 protein, humanToll-Like Receptor 3Tumor Necrosis Factor-alphaAutoimmunityDendritic cellsImmunology

Identifiers

PMID30518680
PMCPMC6328029
OpenAlexW2902524246

What OpenQuestion holds

Textmetadata
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.