Evidence map›Paper›PMID 26592240›Full record

ArticleDiabetologia2016

Human mesenchymal stem cells and derived extracellular vesicles induce regulatory dendritic cells in type 1 diabetic patients.

Enrica Favaro, Andrea Carpanetto, Cristiana Caorsi, Mirella Giovarelli, Costanza Angelini, Paolo Cavallo-Perin, Ciro Tetta, Giovanni Camussi, Maria M Zanone

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

108 citing papers in PubMed, 156 citations in OpenAlex.

  1. Review
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  8. Advancements in diabetes research and stem cell therapy: a concise review.Journal of diabetes and metabolic disorders · 2025
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  10. Article
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  14. Advances in the Role of Stem Cell-Derived Exosomes in Diabetic Foot Wound Healing.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
  15. Review
  16. Review
  17. Article
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  19. Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024
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  20. Review

48 more citing papers are in PubMed but not listed here.

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 at 1 institution in 2 countries.

Enrica FavaroDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126, Torino, Italy.
Andrea CarpanettoDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126, Torino, Italy.
Cristiana CaorsiImmunogenetic and Transplant Biology Laboratory, University of Turin, Turin, Italy.
Mirella GiovarelliDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
Costanza AngeliniDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
Paolo Cavallo-PerinDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126, Torino, Italy.
Ciro TettaTranslational Centre for Regenerative Medicine, University of Turin, Turin, Italy.
Giovanni CamussiDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126, Torino, Italy.
Maria M ZanoneDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126, Torino, Italy. mariamaddalena.zanone@unito.it.
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisMesenchymal stem cells (MSCs) can exert an immunosuppressive effect on any component of the immune system, including dendritic cells (DCs), by direct contact, the release of soluble markers and extracellular vesicles (EVs). We evaluated whether MSCs and MSC-derived EVs have an immunomodulatory effect on monocyte-derived DCs in type 1 diabetes.

methodsBone marrow derived MSCs were characterised and EVs were obtained by ultracentrifugation. DCs were differentiated from CD14(+) cells, obtained from nine type 1 diabetic patients at disease onset, pulsed with antigen GAD65 and cultured with MSCs or EVs. Levels of DC maturation and activation markers were evaluated by flow cytometry. GAD65-pulsed DCs and autologous CD14(-) cell were co-cultured and IFN-γ enzyme-linked immunosorbent spot responses were assayed. Secreted cytokine levels were measured and Th17 and regulatory T cells were analysed.

resultsMSC- and EV-conditioned DCs acquired an immature phenotype with reduced levels of activation markers and increased IL-10 and IL-6 production. Conditioned DC plus T cell co-cultures showed significantly decreased IFN-γ spots and secretion levels. Moreover, higher levels of TGF-β, IL-10 and IL-6 were detected compared with unconditioned DC plus T cell co-cultures. Conditioned DCs decreased Th17 cell numbers and IL-17 levels, and increased FOXP3(+) regulatory T cell numbers. EVs were internalised by DCs and EV-conditioned DCs exhibited a similar effect. CONCLUSIONS/

interpretationIn type 1 diabetes, MSCs induce immature IL-10-secreting DCs in vitro, thus potentially intercepting the priming and amplification of autoreactive T cells in tissue inflammation. These DCs can contribute to the inhibition of inflammatory T cell responses to islet antigens and the promotion of the anti-inflammatory, regulatory responses exerted by MSCs.

Indexed as

Cell DifferentiationDiabetes Mellitus, Type 1AdultCells, CulturedCoculture TechniquesDendritic CellsExtracellular VesiclesFemaleHumansMaleMesenchymal Stem CellsMiddle AgedTh17 CellsT-Lymphocytes, RegulatoryYoung AdultCytokinesDendritic cellsExtracellular vesiclesGADMesenchymal stem cellsProstaglandin E2T cellsType 1 diabetes

Identifiers

PMID26592240
OpenAlexW2180163807

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.