We are analyzing https://link.springer.com/article/10.1186/s13287-022-03219-x.

Title:
Transfer of mesenchymal stem cell mitochondria to CD4+ T cells contributes to repress Th1 differentiation by downregulating T-bet expression | Stem Cell Research & Therapy
Description:
Background Mesenchymal stem/stromal cells (MSCs) are multipotent cells with strong tissue repair and immunomodulatory properties. Due to their ability to repress pathogenic immune responses, and in particular T cell responses, they show therapeutic potential for the treatment of autoimmune diseases, organ rejection and graft versus host disease. MSCs have the remarkable ability to export their own mitochondria to neighboring cells in response to injury and inflammation. However, whether mitochondrial transfer occurs and has any role in the repression of CD4+ Th1 responses is unknown. Methods and results In this report we have utilized CD4+ T cells from HNT TCR transgenic mice that develop Th1-like responses upon antigenic stimulation in vitro and in vivo. Allogeneic bone marrow-derived MSCs reduced the diabetogenic potential of HNT CD4+ T cells in vivo in a transgenic mouse model of disease. In co-culture experiments, we have shown that MSCs were able to reduce HNT CD4+ T cell expansion, expression of key effector markers and production of the effector cytokine IFNγ after activation. This was associated with the ability of CD4+ T cells to acquire mitochondria from MSCs as evidenced by FACS and confocal microscopy. Remarkably, transfer of isolated MSC mitochondria to CD4+ T cells resulted in decreased T cell proliferation and IFNγ production. These effects were additive with those of prostaglandin E2 secreted by MSCs. Finally, we demonstrated that both co-culture with MSCs and transfer of isolated MSC mitochondria prevent the upregulation of T-bet, the master Th1 transcription factor, on activated CD4+ T cells. Conclusion The present study demonstrates that transfer of MSC mitochondria to activated CD4+ T cells results in the suppression of Th1 responses in part by downregulating T-bet expression. Furthermore, our studies suggest that MSC mitochondrial transfer might represent a general mechanism of MSC-dependent immunosuppression.
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Keywords {🔍}

cells, cell, mscs, hnt, mitochondria, article, google, scholar, activated, transfer, msc, msca, stem, fig, mesenchymal, cas, mitochondrial, expression, tbet, ifnγ, responses, experiments, pge, presence, human, mice, proliferation, cultured, anticd, data, effects, immunol, activation, harvested, differentiation, results, coculture, shown, facs, immunosuppressive, values, effector, isolated, sem, vivo, production, mitoception, mitotracker, additional, function,

Topics {✒️}

tailed mann–whitney u-test fas ligand regulates ha-specific mhc class pro-inflammatory cytokines transfer 4 μm pore size inserts protease/phosphatase inhibitor cocktail regulatory t-cell generation scale bar 10 μm article google scholar downregulating t-bet expression hla-dependent manner improving ram-saint eloi platform expanded antigen-specific tregs downregulated t-bet expression promote t-cell tolerance full size image restore antigen-specific tolerance 50 ng/ml phorbolmyristate acetate t-bet downregulation contributes mesenchymal stem cells anti-cd4-percp-cy5-5 cell t-bet expression cell-mediated spontaneous diabetes mesenchymal stromal cells anti-cd3/cd28 activated cd4+ prevented t-bet upregulation compared t-bet expression t-bet expression modulation mscs upregulate pd-l1 mitotracker deep red priming msc-mediated suppression anti-cd25-pe-cy7 article download pdf cell-based therapy human induced tregs ice-cold mannitol buffer cfse-labeled hnt cd4+ cell stem cell mitotracker-labeled msc mitochondria assessed t-bet expression mitotracker red cmxros full access blood glucose levels systemic lupus erythematosus hepatocyte growth factor bone marrow antigen-specific tolerance privacy choices/manage cookies inflammatory bowel disease inflammatory bowels disease

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         description:Mesenchymal stem/stromal cells (MSCs) are multipotent cells with strong tissue repair and immunomodulatory properties. Due to their ability to repress pathogenic immune responses, and in particular T cell responses, they show therapeutic potential for the treatment of autoimmune diseases, organ rejection and graft versus host disease. MSCs have the remarkable ability to export their own mitochondria to neighboring cells in response to injury and inflammation. However, whether mitochondrial transfer occurs and has any role in the repression of CD4+ Th1 responses is unknown. In this report we have utilized CD4+ T cells from HNT TCR transgenic mice that develop Th1-like responses upon antigenic stimulation in vitro and in vivo. Allogeneic bone marrow-derived MSCs reduced the diabetogenic potential of HNT CD4+ T cells in vivo in a transgenic mouse model of disease. In co-culture experiments, we have shown that MSCs were able to reduce HNT CD4+ T cell expansion, expression of key effector markers and production of the effector cytokine IFNγ after activation. This was associated with the ability of CD4+ T cells to acquire mitochondria from MSCs as evidenced by FACS and confocal microscopy. Remarkably, transfer of isolated MSC mitochondria to CD4+ T cells resulted in decreased T cell proliferation and IFNγ production. These effects were additive with those of prostaglandin E2 secreted by MSCs. Finally, we demonstrated that both co-culture with MSCs and transfer of isolated MSC mitochondria prevent the upregulation of T-bet, the master Th1 transcription factor, on activated CD4+ T cells. The present study demonstrates that transfer of MSC mitochondria to activated CD4+ T cells results in the suppression of Th1 responses in part by downregulating T-bet expression. Furthermore, our studies suggest that MSC mitochondrial transfer might represent a general mechanism of MSC-dependent immunosuppression.
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      description:Mesenchymal stem/stromal cells (MSCs) are multipotent cells with strong tissue repair and immunomodulatory properties. Due to their ability to repress pathogenic immune responses, and in particular T cell responses, they show therapeutic potential for the treatment of autoimmune diseases, organ rejection and graft versus host disease. MSCs have the remarkable ability to export their own mitochondria to neighboring cells in response to injury and inflammation. However, whether mitochondrial transfer occurs and has any role in the repression of CD4+ Th1 responses is unknown. In this report we have utilized CD4+ T cells from HNT TCR transgenic mice that develop Th1-like responses upon antigenic stimulation in vitro and in vivo. Allogeneic bone marrow-derived MSCs reduced the diabetogenic potential of HNT CD4+ T cells in vivo in a transgenic mouse model of disease. In co-culture experiments, we have shown that MSCs were able to reduce HNT CD4+ T cell expansion, expression of key effector markers and production of the effector cytokine IFNγ after activation. This was associated with the ability of CD4+ T cells to acquire mitochondria from MSCs as evidenced by FACS and confocal microscopy. Remarkably, transfer of isolated MSC mitochondria to CD4+ T cells resulted in decreased T cell proliferation and IFNγ production. These effects were additive with those of prostaglandin E2 secreted by MSCs. Finally, we demonstrated that both co-culture with MSCs and transfer of isolated MSC mitochondria prevent the upregulation of T-bet, the master Th1 transcription factor, on activated CD4+ T cells. The present study demonstrates that transfer of MSC mitochondria to activated CD4+ T cells results in the suppression of Th1 responses in part by downregulating T-bet expression. Furthermore, our studies suggest that MSC mitochondrial transfer might represent a general mechanism of MSC-dependent immunosuppression.
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            name:CHU Montpellier
            address:
               name:CHU Montpellier, Montpellier, France
               type:PostalAddress
            type:Organization
      name:Marie-Luce Vignais
      affiliation:
            name:Université de Montpellier
            address:
               name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
               type:PostalAddress
            type:Organization
            name:Université de Montpellier
            address:
               name:IGF, CNRS, INSERM, Université de Montpellier, Montpellier, France
               type:PostalAddress
            type:Organization
      name:Javier Hernandez
      url:http://orcid.org/0000-0002-7218-7519
      affiliation:
            name:Université de Montpellier
            address:
               name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:IGF, CNRS, INSERM, Université de Montpellier, Montpellier, France
      name:IGMM, CNRS, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:INM, INSERM, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:CHU Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France
      name:IGF, CNRS, INSERM, Université de Montpellier, Montpellier, France
      name:Institute for Regenerative Medicine and Biotherapy (IRMB), INSERM U1183, Université de Montpellier, Montpellier, France

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