ArticleFrontiers in immunology2012
Rat mesenchymal stromal cells inhibit T cell proliferation but not cytokine production through inducible nitric oxide synthase.
Article in Frontiers in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Nitric Oxide in the Intestinal Stem Cell Niche: A Spatial Model of Nitrosative Stress and Clonal Evolution in Colitis-Associated Colorectal Cancer.Digestive diseases and sciences · 2026Review
- Bidirectional role of neutrophils in tumor development.Molecular cancer · 2025Review
- Nitric oxide modulation in neuroinflammation and the role of mesenchymal stem cells.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- A procedure for in vitro evaluation of the immunosuppressive effect of mouse mesenchymal stem cells on activated T cell proliferation.Stem cell research & therapy · 2021Article
- Engineering the MSC Secretome: A Hydrogel Focused Approach.Advanced healthcare materials · 2021Review
- Functional Characteristics and Application of Mesenchymal Stem Cells in Systemic Lupus Erythematosus.Archivum immunologiae et therapiae experimentalis · 2021Review
- Mesenchymal Stem Cells Reverse Diabetic Nephropathy Disease via Lipoxin A4 by Targeting Transforming Growth Factor β (TGF-β)/smad Pathway and Pro-Inflammatory Cytokines.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Bone marrow-derived mesenchymal stromal cells promote colorectal cancer cell death under low-dose irradiation.British journal of cancer · 2018Article
- Cancer stem cell niche models and contribution by mesenchymal stroma/stem cells.Molecular cancer · 2017Review
- Heparan Sulfate: A Potential Candidate for the Development of Biomimetic Immunomodulatory Membranes.Frontiers in bioengineering and biotechnology · 2017Article
- Chondroitin Sulfate Immobilized on a Biomimetic Scaffold Modulates Inflammation While Driving Chondrogenesis.Stem cells translational medicine · 2016Article
- Defining novel parameters for the optimal priming and expansion of minor histocompatibility antigen-specific T cells in culture.Journal of translational medicine · 2015Article
- Phylogenetic distinction of iNOS and IDO function in mesenchymal stem cell-mediated immunosuppression in mammalian species.Cell death and differentiation · 2014Article
- Mesenchymal stem cells: are we ready for clinical application in transplantation and tissue regeneration?Frontiers in immunology · 2013Article
- Mesenchymal stem cells as all-round supporters in a normal and neoplastic microenvironment.Cell communication and signaling : CCS · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesenchymal stromal cells (MSC) have important immunomodulatory properties, they inhibit T lymphocyte allo-activation and have been used to treat graft-versus-host disease. How MSC exert their immunosuppressive functions is not completely understood but species specific mechanisms have been implicated. In this study we have investigated the mechanisms for rat MSC mediated inhibition of T lymphocyte proliferation and secretion of inflammatory cytokines in response to allogeneic and mitogenic stimuli in vitro. MSC inhibited the proliferation of T cells in allogeneic mixed lymphocyte reactions and in response to mitogen with similar efficacy. The anti-proliferative effect was mediated by the induced expression of nitric oxide (NO) synthase and production of NO by MSC. This pathway was required and sufficient to fully suppress lymphocyte proliferation and depended on proximity of MSC and target cells. Expression of inducible NO synthase by MSC was induced through synergistic stimulation with tumor necrosis factor α and interferon γ secreted by activated lymphocytes. Conversely, MSC had a pronounced inhibitory effect on the secretion of these cytokines by T cells which did not depend on NO synthase activity or cell contact, but was partially reversed by addition of the cyclooxygenase (COX) inhibitor indomethacin. In conclusion, rat MSC use different mechanisms to inhibit proliferative and inflammatory responses of activated T cells. While proliferation is suppressed by production of NO, cytokine secretion appears to be impaired at least in part by COX-dependent production of prostaglandin E(2).
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