Evidence map›Paper›PMID 39114661›Full record

ArticleFrontiers in immunology2024

Extracellular vesicles derived from stressed beta cells mediate monocyte activation and contribute to islet inflammation.

Mette C Dekkers, Joost M Lambooij, Xudong Pu, Raphael R Fagundes, Agustin Enciso-Martinez, Kim Kats, Ben N G Giepmans, Bruno Guigas, Arnaud Zaldumbide

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  15. Car@PLGA-NPs target gut microbiota-ER stress axis to combat diabetes.Frontiers in cellular and infection microbiology · 2025
    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

9 authors.

Mette C Dekkers *Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands.
Joost M Lambooij *Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands.
Xudong PuDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands.
Raphael R FagundesDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands.
Agustin Enciso-MartinezDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands.
Kim KatsDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Ben N G GiepmansDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Bruno Guigas *Leiden University Center of Infectious Diseases, Leiden University Medical Center, Leiden, Netherlands.
Arnaud Zaldumbide *Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Beta cell destruction in type 1 diabetes (T1D) results from the combined effect of inflammation and recurrent autoimmunity. In recent years, the role played by beta cells in the development of T1D has evolved from passive victims of the immune system to active contributors in their own destruction. We and others have demonstrated that perturbations in the islet microenvironment promote endoplasmic reticulum (ER) stress in beta cells, leading to enhanced immunogenicity. Among the underlying mechanisms, secretion of extracellular vesicles (EVs) by beta cells has been suggested to mediate the crosstalk with the immune cell compartment. Methods: To study the role of cellular stress in the early events of T1D development, we generated a novel cellular model for constitutive ER stress by modulating the expression of Results: Analysis of the transcriptome showed that Conclusion: These findings indicate that the content of EVs derived from stressed beta cells can be a mediator of islet inflammation.

Indexed as

Endoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressExtracellular VesiclesInsulin-Secreting CellsMicroRNAsMonocytesAnimalsCell LineDiabetes Mellitus, Type 1HumansInflammationIslets of LangerhansSignal TransductionUnfolded Protein ResponseEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanHspa5 protein, mouseMicroRNAser stressextracellular vesiclesinflammationmonocytestype 1 diabetes

Identifiers

PMID39114661
PMCPMC11303142

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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.