Evidence map›Paper›PMID 36194479›Full record

ArticleJCI insight2022

NLRC4-mediated activation of CD1c+ DC contributes to perpetuation of synovitis in rheumatoid arthritis.

Cristina Delgado-Arévalo, Marta Calvet-Mirabent, Ana Triguero-Martínez, Enrique Vázquez de Luis, Alberto Benguría-Filippini, Raquel Largo, Diego Calzada-Fraile, Olga Popova, Ildefonso Sánchez-Cerrillo, Ilya Tsukalov and 9 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  7. Rheumatoid Arthritis Therapy Based on B Cells.Drug design, development and therapy · 2025
    Review
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  9. Article
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  11. Article
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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

19 authors at 5 institutions in 1 country.

Cristina Delgado-ArévaloImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Marta Calvet-MirabentImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Ana Triguero-MartínezRheumatology Department from Hospital Universitario La Princesa, Instituto de Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Enrique Vázquez de LuisGenomic Unit, The National Centre for Cardiovascular Research, Madrid, Spain.
Alberto Benguría-FilippiniGenomic Unit, The National Centre for Cardiovascular Research, Madrid, Spain.
Raquel LargoBone and Joint Research Unit, Rheumatology Service, IIS Fundación Jiménez Díaz, Madrid, Spain.
Diego Calzada-FraileImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Olga PopovaImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Ildefonso Sánchez-CerrilloImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Ilya TsukalovImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Roberto Moreno-VelliscaGenomic Unit, The National Centre for Cardiovascular Research, Madrid, Spain.
Hortensia de la FuenteImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Gabriel Herrero-BeaumontBone and Joint Research Unit, Rheumatology Service, IIS Fundación Jiménez Díaz, Madrid, Spain.
Almudena RamiroBiology Laboratory, The National Centre for Cardiovascular Research, Madrid, Spain.
Francisco Sánchez-MadridImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Santos CastañedaRheumatology Department from Hospital Universitario La Princesa, Instituto de Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Ana DopazoGenomic Unit, The National Centre for Cardiovascular Research, Madrid, Spain.
Isidoro González ÁlvaroRheumatology Department from Hospital Universitario La Princesa, Instituto de Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Enrique Martin-GayoImmunology Unit from Hospital Universitario La Princesa, Medicine Faculty, Autonomous University of Madrid (UAM), Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain.
Hospital Universitario de La Princesa · ESCentro de Investigación en Red en Enfermedades Cardiovasculares · ESSpanish National Centre for Cardiovascular Research · ESHospital Universitario Fundación Jiménez Díaz · ESCentre for Biomedical Network Research on Rare Diseases · ES

Funding

Tailored induction of HIV-1 specific immunity through engineered dendritic cell vaccinesR21AI140930 · NIAID · UNIVERSIDAD AUTONOMA DE MADRID · PI MARTIN-GAYO, ENRIQUE · 2018 to 2019
$297k
NIAID NIH HHS R21 AI140930
6 · The paper itself

Abstract

The individual contribution of specific myeloid subsets such as CD1c+ conventional DC (cDC) to perpetuation of rheumatoid arthritis (RA) pathology remains unclear. In addition, the specific innate sensors driving pathogenic activation of CD1c+ cDC in patients with RA and their functional implications have not been characterized. Here, we assessed phenotypical, transcriptional, and functional characteristics of CD1c+ and CD141+ cDC and monocytes from the blood and synovial fluid of patients with RA. Increased levels of CCR2 and the IgG receptor CD64 on circulating CD1c+ cDC was associated with the presence of this DC subset in the synovial membrane in patients with RA. Moreover, synovial CD1c+ cDC are characterized by increased expression of proinflammatory cytokines and high abilities to induce pathogenic IFN-γ+IL-17+CD4+ T cells in vitro. Finally, we identified the crosstalk between Fcγ receptors and NLRC4 as a potential molecular mechanism mediating pathogenic activation, CD64 upregulation, and functional specialization of CD1c+ cDC in response to dsDNA-IgG in patients with RA.

Indexed as

Arthritis, RheumatoidDendritic CellsAntigens, CD1Calcium-Binding ProteinsCARD Signaling Adaptor ProteinsCytokinesGlycoproteinsHumansSynovial FluidSynovial MembraneAntigens, CD1Calcium-Binding ProteinsCARD Signaling Adaptor ProteinsCD1C protein, humanCytokinesGlycoproteinsNLRC4 protein, humanAutoimmune diseasesAutoimmunityCell BiologyDendritic cellsInnate immunity

Identifiers

PMID36194479
PMCPMC9746818
OpenAlexW4301178897

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.