Mesenchymal Stromal Cell-Derived Extracellular Vesicles Attenuate Dendritic Cell Maturation and Function
Open accessAbstract
Mesenchymal stromal cells (MSCs) are potent regulators of immune responses largely through paracrine signaling. MSC secreted extracellular vesicles (MSC-EVs) are increasingly recognized as the key paracrine factors responsible for the biological and therapeutic function of MSCs. We report the first comprehensive study demonstrating the immunomodulatory effect of MSC-EVs on dendritic cell (DC) maturation and function. MSC-EVs were isolated from MSC conditioned media using differential ultracentrifugation. Human monocyte-derived DCs were generated in the absence or presence of MSC-EVs (20 ug/ml) then subjected to phenotypic and functional analysis in vitro. MSC-EV treatment impaired antigen uptake by immature DCs and halted DC maturation resulting in reduced expression of the maturation and activation markers CD83, CD38, and CD80, decreased secretion of pro-inflammatory cytokines IL-6 and IL-12p70 and increased production of anti-inflammatory cytokine TGF-β. MSC-EV treated DCs also demonstrated a diminished CCR 7 expression after LPS stimulation, coupled with a significantly reduced ability to migrate towards the CCR7-ligand CCL21, although they were still able to stimulate allogeneic T cell proliferation in vitro. Through microRNA profiling we have identified 49 microRNAs, which were significantly enriched in MSC-EVs compared to their parent MSCs. MicroRNAs with known effect on DC maturation and functions, including miR-21-5p, miR-142-3p, miR-223-3p and miR-126-3p, were detected within the top 10 most enriched miRNAs in MSC-EVs, with MiR-21-5p as the third highest expressed miRNA in MSC-EVs. In silico analysis revealed that miR-21-5p targets the CCR7 gene for degradation. To verify these observations, DCs were transfected with miR-21-5p mimics and analyzed for their ability to migrate towards the CCR7-ligand CCL21 in vitro. MiR-21-5p mimic transfected DCs showed a clear trend of reduced CCR7 expression and a significantly decreased migratory ability towards the CCL21. Our findings suggest that MSC-EVs are able to recapitulate MSC mediated DC modulation and MSC-EV enclosed microRNAs may represent a novel mechanism through which MSCs modulate DC functions. As MSCs are currently used in clinical trials to treat numerous diseases associated with immune dysregulation such as graft-versus-host disease and inflammatory bowel disease, our data provide novel evidence to inform potential future application of MSC-EVs as a cell-free therapeutic agent.
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Some miRNAs present in MSC-derived EVs suppress dendritic cell activity, such as miR-126-3p, miR-223-3p and miR-142-3p.
“some miRNAs present in MSC-derived EVs are capable of suppressing DC activity, such as mi-R-126-3p, miR-223-3p and miR-142-3p [47].”
From Mesenchymal stem cell secretome for regenerative medicine: Where do we stand? (2025) · cites this paper as [47]
The Results section identifies miR-126-3p, miR-223-3p and miR-142-3p among MSC-EV miRNAs with known effects on dendritic-cell maturation and function. But the Discussion describes their role in MSC-EV-mediated modulation as a potential mechanism, and says further studies are needed to establish the impact of miRNAs other than miR-21-5p. The source therefore does not demonstrate that these three MSC-EV miRNAs suppress dendritic-cell activity. (LLM, conf=0.88)
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- Authors
- Reis, M., Mavin, E., Nicholson, L., Green, K., Dickinson, A. M., & Wang, X.-N.
- Affiliations
- Newcastle University (GB)
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2018-11-09
- Volume
- 9
- Pages
- 2538-2538
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6237916
- OpenAlex
- W2896358322
- Cited by
- 286
- References
- 63
- Citations by year
- 2026: 26 · 2025: 37 · 2024: 36 · 2023: 47 · 2022: 41 · 2021: 49 · 2020: 33 · 2019: 16
- FWCI
- 8.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- National Institute for Health and Care Research
- Newcastle University
- European Commission (315963)
- Versus Arthritis (19429)
- NIHR Newcastle Biomedical Research Centre
- FP7 People: Marie-Curie Actions
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- mesenchymal stem cells, extracellular vesicles, dendritic cell maturation, immunomodulation, microRNA, miR-21-5p, CCR7, CCL21, dendritic cell migration, antigen uptake, inflammatory cytokines, TGF-beta, paracrine signaling, conditioned medium, allogeneic T cell proliferation
- MeSH terms
- Extracellular Vesicles, Cell Differentiation, Cells, Cultured, Dendritic Cells, Graft vs Host Disease, Humans, Inflammation, Interleukin-6, Cytokines, Transforming Growth Factor beta, Interleukin-12, MicroRNAs, Cell Proliferation, Receptors, CCR7, Chemokine CCL21, Mesenchymal Stem Cells
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