Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells
Open accessAbstract
There has been a marked increase in the incidence of autoimmune diseases in the past half-century. Although the underlying genetic basis of this class of diseases has recently been elucidated, implicating predominantly immune-response genes, changes in environmental factors must ultimately be driving this increase. The newly identified population of interleukin (IL)-17-producing CD4(+) helper T cells (TH17 cells) has a pivotal role in autoimmune diseases. Pathogenic IL-23-dependent TH17 cells have been shown to be critical for the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, and genetic risk factors associated with multiple sclerosis are related to the IL-23-TH17 pathway. However, little is known about the environmental factors that directly influence TH17 cells. Here we show that increased salt (sodium chloride, NaCl) concentrations found locally under physiological conditions in vivo markedly boost the induction of murine and human TH17 cells. High-salt conditions activate the p38/MAPK pathway involving nuclear factor of activated T cells 5 (NFAT5; also called TONEBP) and serum/glucocorticoid-regulated kinase 1 (SGK1) during cytokine-induced TH17 polarization. Gene silencing or chemical inhibition of p38/MAPK, NFAT5 or SGK1 abrogates the high-salt-induced TH17 cell development. The TH17 cells generated under high-salt conditions display a highly pathogenic and stable phenotype characterized by the upregulation of the pro-inflammatory cytokines GM-CSF, TNF-α and IL-2. Moreover, mice fed with a high-salt diet develop a more severe form of EAE, in line with augmented central nervous system infiltrating and peripherally induced antigen-specific TH17 cells. Thus, increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases through the induction of pathogenic TH17 cells.
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Gene silencing or chemical inhibition of p38/MAPK, NFAT5, or SGK1 can negate development of Th17 cells induced by high salt environments.
“Gene silencing or chemical inhibition of p38/MAPK, NFAT5, or SGK1 can negate the development of Th17 cells induced by high salt environments”
From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Kleinewietfeld et al., 2013
Extracellular salt (NaCl) can influence TH17 homeostasis, and short-chain fatty acids can influence Treg homeostasis.
“Added to this are recent results indicating that extracellular salt (NaCl) (37, 38) and short-chain fatty acids (39) can influence TH17 and Treg homeostasis, respectively.”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [38]
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- Authors
- Kleinewietfeld, M., Manzel, A., Titze, J., Kvakan, H., Yosef, N., Linker, R. A., Muller, D. N., & Hafler, D. A.
- Affiliations
- Yale University (US)
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- Max Delbrück Center (DE)
- Broad Institute (US)
- Corresponding author
- Kleinewietfeld, Markus
- Hafler, David A.
- Venue
- Nature
- Published
- 2013-03-06
- Volume
- 496
- Issue
- 7446
- Pages
- 518-522
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3746493
- OpenAlex
- W2154911070
- Cited by
- 1,394
- References
- 42
- Citations by year
- 2026: 60 · 2025: 76 · 2024: 99 · 2023: 93 · 2022: 113 · 2021: 113 · 2020: 126 · 2019: 111 · 2018: 92 · 2017: 135 · 2016: 100 · 2015: 104 · 2014: 107 · 2013: 61
- FWCI
- 68.63
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
- Funders
- Multiple Sclerosis Society
- National Institute of Allergy and Infectious Diseases (U19AI070352, U19AI046130, P01AI045757, U01AI102011, R01AI091568, P01AI039671)
- National Institute of Neurological Disorders and Stroke (NS2427, R01NS024247)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Physical Sciences › Environmental Science › Pollution › Thallium and Germanium Studies
- Keywords
- high-salt diet, sodium chloride, Th17 cells, experimental autoimmune encephalomyelitis, multiple sclerosis, p38 MAPK, NFAT5, SGK1, IL-17, CD4+ T cells, IL-23, autoimmune disease, environmental risk factors, neuroinflammation, gene regulatory networks, salt intake
- MeSH terms
- Serum-Glucocorticoid Regulated Kinases, Animals, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Humans, Interleukin-2, Mice, Inbred C57BL, Phenotype, Transcription Factors, Tumor Necrosis Factor-alpha, Granulocyte-Macrophage Colony-Stimulating Factor, Protein Serine-Threonine Kinases, Sodium Chloride, Dietary, Immediate-Early Proteins, Gene Silencing, MAP Kinase Signaling System, p38 Mitogen-Activated Protein Kinases, Mice, Th17 Cells
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