Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells

Markus Kleinewietfeld (), Arndt Manzel, Jens Titze, Heda Kvakan, Nir Yosef, Ralf A. Linker, Dominik N. Muller and David A. Hafler ()
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Markus Kleinewietfeld: Yale School of Medicine, 15 York Street, New Haven, Connecticut 06520, USA
Arndt Manzel: University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany
Jens Titze: Vanderbilt University, 2213 Garland Avenue, Nashville, Tennessee 37232, USA
Heda Kvakan: Experimental and Clinical Research Center, a joint cooperation between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine, Lindenberger Weg 80, 13125 Berlin, Germany
Nir Yosef: Broad Institute of MIT and Harvard, 7 Cambridge Center
Ralf A. Linker: University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany
Dominik N. Muller: Experimental and Clinical Research Center, a joint cooperation between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine, Lindenberger Weg 80, 13125 Berlin, Germany
David A. Hafler: Yale School of Medicine, 15 York Street, New Haven, Connecticut 06520, USA

Nature, 2013, vol. 496, issue 7446, 518-522

Abstract: Increased salt concentrations are shown to induce murine and human TH17 cells by a mechanism that depends on activation of p38/MAPK, NFAT5 and SGK1; mice kept on a high-salt diet develop a more severe experimental autoimmune encephalomyelitis due to increased induction of TH17 cells.

Date: 2013
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DOI: 10.1038/nature11868

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