Salt generates antiinflammatory Th17 cells but amplifies pathogenicity in proinflammatory cytokine microenvironments
Th cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to acc...
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| Vydáno v: | The Journal of clinical investigation Ročník 130; číslo 9; s. 4587 - 4600 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
American Society for Clinical Investigation
01.09.2020
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| ISSN: | 0021-9738, 1558-8238, 1558-8238 |
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| Abstract | Th cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here, we demonstrate that high-NaCl conditions induced a stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and IL-17A expression in high-NaCl conditions. The NaCl-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high-NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a proinflammatory and TGF-β-low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs. |
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| AbstractList | Th cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here, we demonstrate that high-NaCl conditions induced a stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and IL-17A expression in high-NaCl conditions. The NaCl-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high-NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a proinflammatory and TGF-β-low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs.Th cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here, we demonstrate that high-NaCl conditions induced a stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and IL-17A expression in high-NaCl conditions. The NaCl-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high-NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a proinflammatory and TGF-β-low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs. Th cells Integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here, we demonstrate that high-NaCl conditions induced a stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and IL-17A expression in high-NaCl conditions. The NaCl-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high-NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a proinflammatory and TGF-[beta]-low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs. Th cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here, we demonstrate that high-NaCl conditions induced a stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and IL-17A expression in high-NaCl conditions. The NaCl-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high-NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a proinflammatory and TGF-ß-low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs. Th cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here, we demonstrate that high-NaCl conditions induced a stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and IL-17A expression in high-NaCl conditions. The NaCl-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high-NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a proinflammatory and TGF-β–low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs. |
| Audience | Academic |
| Author | Matthias, Julia Jacobsen, Ilse D. Picard, Felix Floess, Stefan Peters, Anneli Korn, Thomas Huehn, Jochen Glasmacher, Elke Baumjohann, Dirk de Almeida, Gustavo P. Huber, Magdalena Kolz, Anna Zielinski, Christina E. Zeiträg, Julia Riedel, Thomas Heink, Sylvia Chao, Ying-Yin Soll, Dominik |
| AuthorAffiliation | 2 German Center for Infection Research, Partner Site Munich, Munich, Germany 13 Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures, Braunschweig and German Center for Infection Research, Partner Site Hannover-Braunschweig, Hannover-Braunschweig, Germany 4 Klinikum rechts der Isar, Department of Experimental Neuroimmunology, Technical University of Munich, Munich, Germany 5 Munich Cluster for Systems Neurology (SyNergy), Munich, Germany 10 Roche Innovation Center Munich, pRED, Large Molecule Research, Penzberg, Germany 11 Research Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology – Hans Knöll Institute, Jena, Germany 12 Institute of Microbiology, Friedrich Schiller University, Jena, Germany 1 Institute of Virology, Technical University of Munich, Munich, Germany 9 TranslaTUM, Technical University of Munich, Munich, Germany 7 Institute for Immunology, Biomedical Center, Faculty of Medicine, Ludwig Maximilian University of Mu |
| AuthorAffiliation_xml | – name: 1 Institute of Virology, Technical University of Munich, Munich, Germany – name: 10 Roche Innovation Center Munich, pRED, Large Molecule Research, Penzberg, Germany – name: 12 Institute of Microbiology, Friedrich Schiller University, Jena, Germany – name: 6 Institute for Medical Microbiology and Hygiene, University of Marburg, Marburg, Germany – name: 2 German Center for Infection Research, Partner Site Munich, Munich, Germany – name: 8 Institute of Clinical Neuroimmunology, Hospital and Biomedical Center of LMU Munich, Planegg-Martinsried, Germany – name: 13 Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures, Braunschweig and German Center for Infection Research, Partner Site Hannover-Braunschweig, Hannover-Braunschweig, Germany – name: 3 Department of Cellular Immunoregulation, Charité – Universitätsmedizin Berlin, Berlin, Germany – name: 11 Research Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology – Hans Knöll Institute, Jena, Germany – name: 9 TranslaTUM, Technical University of Munich, Munich, Germany – name: 5 Munich Cluster for Systems Neurology (SyNergy), Munich, Germany – name: 4 Klinikum rechts der Isar, Department of Experimental Neuroimmunology, Technical University of Munich, Munich, Germany – name: 14 Department of Experimental Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany – name: 7 Institute for Immunology, Biomedical Center, Faculty of Medicine, Ludwig Maximilian University of Munich (LMU Munich), Planegg-Martinsried, Germany |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32484796$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Anti-inflammatory agents Autoimmunity Biomedical research Bone morphogenetic proteins Cell fate Cellular Microenvironment - drug effects Cellular Microenvironment - immunology Cloning Cytokines Cytokines - genetics Cytokines - immunology Dietary intake Experimental allergic encephalomyelitis Foxp3 protein Genotype & phenotype Helper cells Humans Immunological tolerance Inflammation - genetics Inflammation - immunology Inflammation - pathology Inflammatory diseases Lymphocytes Lymphocytes T MAP kinase MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - genetics MAP Kinase Signaling System - immunology Mice Mice, Transgenic Microenvironments Pathogenicity Pathogens Scientific equipment industry Sodium chloride Sodium Chloride, Dietary - pharmacology Software industry Specialization T cell receptors T cells Th17 Cells - immunology Th17 Cells - pathology Transforming growth factors |
| Title | Salt generates antiinflammatory Th17 cells but amplifies pathogenicity in proinflammatory cytokine microenvironments |
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