We are analyzing https://link.springer.com/article/10.1186/s13287-019-1307-9.

Title:
Mesenchymal stem cell repression of Th17 cells is triggered by mitochondrial transfer | Stem Cell Research & Therapy
Description:
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+CCR6+CD45RO+ T helper 17 (Th17) cells by confocal microscopy and fluorescent-activated cell sorting (FACS). We then evaluated the Th17 cell inflammatory phenotype and bioenergetics at 4 h and 24 h of co-culture with BM-MSCs. We found that Th17 cells can take up mitochondria from BM-MSCs already after 4 h of co-culture. Moreover, IL-17 production by Th17 cells co-cultured with BM-MSCs was significantly impaired in a contact-dependent manner. This inhibition was associated with oxygen consumption increase by Th17 cells and interconversion into T regulatory cells. Finally, by co-culturing human synovial MSCs (sMSCs) from patients with rheumatoid arthritis (RA) with Th17 cells, we found that compared with healthy BM-MSCs, mitochondrial transfer to Th17 cells was impaired in RA-sMSCs. Moreover, artificial mitochondrial transfer also significantly reduced IL-17 production by Th17 cells. 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.
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Keywords {🔍}

cells, cell, transfer, bmmscs, mitochondrial, mitochondria, mscs, coculture, article, stem, fig, google, scholar, mesenchymal, donors, msc, bmmsc, cas, human, mitoception, data, healthy, function, cocultured, treg, flow, isolated, activation, mito, expression, effect, france, foxp, analysis, cytometry, mitotracker, jorgensen, phenotype, proliferation, tnfα, experiments, quantification, results, rasmscs, metabolic, metabolism, ifnγ, pbmcs, anticd, mtdna,

Topics {✒️}

pi3k/akt/mtorc1 signaling pathway interleukin-1beta-dependent glycolytic pathway jean-marc brondello primary human cd4+ccr6+cd45r0+ anti-cd28 antibody-coated beads mitotracker-labeled bm-mscs pre-activated anti-foxp3 pe-conjugated mab anti-cd28 monoclonal antibody noymar luque-campos article luz-crawford variable d-loop regions high-throughput sanger strategy andres caicedo article download pdf pe-conjugated anti-ccr6 anti-cd3/cd28 antibodies parametric mann–whitney test fluo-conjugated anti-cd3 mitochondrial rho-gtpase miro tissue-resident immune cells t-cell differentiation facs-sorted cd4+ccr6+cd45ro+ mesenchymal stem cells fluorochrome-conjugated mabs diluted tnf-α/ifn-γ stimulation stromal stem cells mitotracker-labeled bm-mscs isolated anti-ifn-γ–apccy7 tnf-α/ifn-γ activation fluorescent-activated cell sorting mitotracker-positive th17 cells anti-il-cd25–apc il-6-dependent pge2 secretion primary cd4+ccr6+cd45ro+ 1 ng/ml basic fgf induce pro-inflammatory mechanisms cell–cell contacts bm-msc inhibitory effect msc immunomodulatory properties bm-msc mitochondrial dna th17 cells regulates bm-mscs significantly increases cd4+ccr6+cd25highfoxp3+ cells full size image pro-inflammatory th17 cells bm-mscs pre-activated anti-/cd28 antibodies regenerate damaged tissue induce cd4+cd25highfoxp3+ regulatory il-17-producing th17 cells

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      description: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+CCR6+CD45RO+ T helper 17 (Th17) cells by confocal microscopy and fluorescent-activated cell sorting (FACS). We then evaluated the Th17 cell inflammatory phenotype and bioenergetics at 4 h and 24 h of co-culture with BM-MSCs. We found that Th17 cells can take up mitochondria from BM-MSCs already after 4 h of co-culture. Moreover, IL-17 production by Th17 cells co-cultured with BM-MSCs was significantly impaired in a contact-dependent manner. This inhibition was associated with oxygen consumption increase by Th17 cells and interconversion into T regulatory cells. Finally, by co-culturing human synovial MSCs (sMSCs) from patients with rheumatoid arthritis (RA) with Th17 cells, we found that compared with healthy BM-MSCs, mitochondrial transfer to Th17 cells was impaired in RA-sMSCs. Moreover, artificial mitochondrial transfer also significantly reduced IL-17 production by Th17 cells. 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.
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