NDLI: Mesenchymal stem cells inhibit human Th17 cell differentiation and function and induce a T regulatory cell phenotype.

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Mesenchymal stem cells inhibit human Th17 cell differentiation and function and induce a T regulatory cell phenotype.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Pène, Jérôme Torcy-Moquet, Gabriel Yssel, Hans Jorgensen, Christian Ghannam, Soufiane Moquet-Torcy, Gabriel
Description	Country affiliation: France Author Affiliation: Ghannam S ( Institut National de la Santé et de la Recherche Médicale, Unité 844, Hôpital St. Eloi, Université Montpellier I, France.)
Abstract	Mesenchymal stem cells (MSCs) exert immunomodulatory properties via the inhibition of T cell activation and proliferation. Because of the deleterious role of Th17 cells in the pathogenesis of inflammatory disease, we investigated whether proinflammatory cytokines could modify the expression of adhesion molecules on human MSCs, thereby contributing to increased Th17 cell adhesion to MSCs and, as a consequence, modulating the function of the latter cells. IFN-gamma and TNF-alpha synergistically enhanced the expression of CD54 by MSCs, enabling the CCR6 chemokine ligand CCL20 to induce in vitro adhesion of Th17 cells to MSCs. MSCs prevented the in vitro differentiation of naive CD4(+) T cells into Th17 cells and inhibited the production of IL-17, IL-22, IFN-gamma, and TNF-alpha by fully differentiated Th17 cells; this was mediated, in part, via PGE(2), the production of which was enhanced in cocultures with Th17 cells. Moreover, MSCs induced the production of IL-10 and trimethylation of histone H3K4me3 at the promoter of the FOXP3 gene locus, whereas it suppressed trimethylation of the corresponding region in the RORC gene in Th17 cells. These epigenetic changes were associated with the induction of fork head box p3 and the acquisition by Th17 cells of the capacity to inhibit in vitro proliferative responses of activated CD4(+) T cells, which was enhanced when MSCs were preincubated with IFN-gamma and TNF-alpha. These results showed that, under inflammatory conditions, MSCs mediate the adhesion of Th17 cells via CCR6 and exert anti-inflammatory effects through the induction of a T cell regulatory phenotype in these cells.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	1
Volume Number	185
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Immunology Growth Inhibitors Physiology Interleukin-17 Antagonists & Inhibitors Mesenchymal Stromal Cells T-lymphocytes, Helper-inducer Cytology T-lymphocytes, Regulatory Metabolism Animals Antigens, Cd11a Antigens, Cd18 Bone Marrow Cells Cell Adhesion Cell Communication Cell Movement Cells, Cultured Coculture Techniques Immunophenotyping Inflammation Mediators Intercellular Adhesion Molecule-1 Biosynthesis Interferon-gamma L Cells (cell Line) Ligands Pathology Mice Receptors, Ccr6 Tumor Necrosis Factor-alpha Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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