Mesenchymal stem cell repression of Th17 cells is triggered by mitochondrial transfer.
Arthritis, Rheumatoid
/ metabolism
Bone Marrow Cells
/ cytology
Cells, Cultured
Coculture Techniques
Humans
Interleukin-17
/ metabolism
Mesenchymal Stem Cells
/ cytology
Mitochondria
/ metabolism
Oxygen Consumption
Synovial Membrane
/ cytology
T-Lymphocytes, Regulatory
/ cytology
Th17 Cells
/ cytology
Tumor Necrosis Factor-alpha
/ pharmacology
Immunomodulation
Mesenchymal stem cells
Mitochondria transfer
T cell
Th17
Journal
Stem cell research & therapy
ISSN: 1757-6512
Titre abrégé: Stem Cell Res Ther
Pays: England
ID NLM: 101527581
Informations de publication
Date de publication:
01 08 2019
01 08 2019
Historique:
received:
12
01
2019
accepted:
18
06
2019
revised:
13
06
2019
entrez:
3
8
2019
pubmed:
3
8
2019
medline:
17
7
2020
Statut:
epublish
Résumé
Mesenchymal stem cells (MSCs) are multipotent cells with broad immunosuppressive capacities. Recently, it has been reported that MSCs can transfer mitochondria to various cell types, including fibroblast, cancer, and endothelial cells. It has been suggested that mitochondrial transfer is associated with a physiological response to cues released by damaged cells to restore and regenerate damaged tissue. However, the role of mitochondrial transfer to immune competent cells has been poorly investigated. Here, we analyzed the capacity of MSCs from the bone marrow (BM) of healthy donors (BM-MSCs) to transfer mitochondria to primary CD4 The present study brings some insights into a novel mechanism of T cell function regulation through mitochondrial transfer from stromal stem cells. The reduced mitochondrial transfer by RA-sMSCs might contribute to the persistence of chronic inflammation in RA synovitis.
Sections du résumé
BACKGROUND
Mesenchymal stem cells (MSCs) are multipotent cells with broad immunosuppressive capacities. Recently, it has been reported that MSCs can transfer mitochondria to various cell types, including fibroblast, cancer, and endothelial cells. It has been suggested that mitochondrial transfer is associated with a physiological response to cues released by damaged cells to restore and regenerate damaged tissue. However, the role of mitochondrial transfer to immune competent cells has been poorly investigated.
METHODS AND RESULTS
Here, we analyzed the capacity of MSCs from the bone marrow (BM) of healthy donors (BM-MSCs) to transfer mitochondria to primary CD4
CONCLUSIONS
The present study brings some insights into a novel mechanism of T cell function regulation through mitochondrial transfer from stromal stem cells. The reduced mitochondrial transfer by RA-sMSCs might contribute to the persistence of chronic inflammation in RA synovitis.
Identifiants
pubmed: 31370879
doi: 10.1186/s13287-019-1307-9
pii: 10.1186/s13287-019-1307-9
pmc: PMC6676586
doi:
Substances chimiques
Interleukin-17
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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