Evidence map›Paper›PMID 39920698›Full record

ArticleCell communication and signaling : CCS2025

Promoting ER stress in a plasmacytoid dendritic cell line drives fibroblast activation.

Beatriz H Ferreira, Inês S Silva, Andreia Mendes, Fátima Leite-Pinheiro, Adrienne W Paton, James C Paton, Iola F Duarte, Philippe Pierre, Catarina R Almeida

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In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Multifaceted regulation of immune cells in radiation-induced pulmonary fibrosis: from mechanistic insights to targeted therapies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  5. Review
  6. 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

9 authors.

Beatriz H FerreiraInstitute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal.
Inês S SilvaInstitute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal.
Andreia MendesInstitute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal.
Fátima Leite-PinheiroInstitute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal.
Adrienne W PatonDepartment of Molecular and Biomedical Science, Research Centre for Infectious Diseases, University of Adelaide, Adelaide, Australia.
James C PatonDepartment of Molecular and Biomedical Science, Research Centre for Infectious Diseases, University of Adelaide, Adelaide, Australia.
Iola F DuarteCICECO - Aveiro Institute of Materials, Department of Chemistry, University of Aveiro, Aveiro, Portugal.
Philippe PierreInstitute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal.
Catarina R AlmeidaInstitute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, Aveiro, Portugal. cra@ua.pt.

Funding

Fundação para a Ciência e a Tecnologia DOI 10.54499/UIDB/04501/2020Fundação para a Ciência e a Tecnologia UIDB/50011/2020World Scleroderma Foundation and Edith Busch Stiftung the EBF and WSF Research Grant Programme 2022-2023 - MAPFib
6 · The paper itself

Abstract

backgroundFibrosis remains a major complication in several chronic diseases, including systemic sclerosis (SSc). Plasmacytoid dendritic cells (pDCs) are innate immune cells that play a key role in the development of fibrosis in SSc patients, through still poorly defined mechanisms. Interestingly, endoplasmic reticulum (ER) stress signaling pathways are dysregulated in pDCs from patients with SSc, but their contribution to fibrosis remains unclear. Thus, this study aimed to unravel the mechanisms behind the involvement of pDCs and ER stress in fibrosis.

methodsTo address this question, we established an in vitro model designed to study the interactions between pDCs and fibroblasts. More specifically, IMR-90 fibroblasts were co-cultured with CAL-1, a pDC cell line. ER stress was then induced by the bacterial toxin SubAB. Extracellular matrix (ECM) production was assessed using immunoblotting, qPCR and confocal microscopy. The importance of cell-to-cell contact was investigated using conditioned media (CM) and transwell assays.

resultsDirect contact of CAL-1 and IMR-90 cells under ER stress conditions led to increased expression of fibronectin and alpha-smooth muscle actin (α-SMA). This effect required expression of the ER stress signaling sensor protein kinase R-like ER kinase (PERK) in pDCs and was observed only upon direct contact between both cell types.

conclusionsOverall, our data suggest that ER stress induction in pDCs promotes fibroblast activation, which may contribute to the development of fibrosis in SSc.

Indexed as

Dendritic CellsEndoplasmic Reticulum StressFibroblastsActinsCell CommunicationCell LineeIF-2 KinaseExtracellular MatrixFibronectinsFibrosisHumansSignal TransductionActinseIF-2 KinaseFibronectinsCell-cell communicationER stressFibroblastsFibrosisInterstitial lung diseasePERKPlasmacytoid dendritic cellsSclerodermaUPR

Identifiers

PMID39920698
PMCPMC11804055

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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.