Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1
Open accessAbstract
TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that are critical for clearing extracellular pathogens and for inducing multiple autoimmune diseases. IL-23 has a critical role in stabilizing and reinforcing the TH17 phenotype by increasing expression of IL-23 receptor (IL-23R) and endowing TH17 cells with pathogenic effector functions. However, the precise molecular mechanism by which IL-23 sustains the TH17 response and induces pathogenic effector functions has not been elucidated. Here we used transcriptional profiling of developing TH17 cells to construct a model of their signalling network and nominate major nodes that regulate TH17 development. We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase, as an essential node downstream of IL-23 signalling. SGK1 is critical for regulating IL-23R expression and stabilizing the TH17 cell phenotype by deactivation of mouse Foxo1, a direct repressor of IL-23R expression. SGK1 has been shown to govern Na(+) transport and salt (NaCl) homeostasis in other cells. We show here that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity. Loss of SGK1 abrogated Na(+)-mediated TH17 differentiation in an IL-23-dependent manner. These data demonstrate that SGK1 has a critical role in the induction of pathogenic TH17 cells and provide a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers TH17 development and promotes tissue inflammation.
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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 [37]
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- Authors
- Wu, C., Yosef, N., Thalhamer, T., Zhu, C., Xiao, S., Kishi, Y., Regev, A., & Kuchroo, V. K.
- Affiliations
- Brigham and Women's Hospital (US)
- Broad Institute (US)
- Corresponding author
- Regev, Aviv
- Kuchroo, Vijay K.
- Venue
- Nature
- Published
- 2013-03-06
- Volume
- 496
- Issue
- 7446
- Pages
- 513-517
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3637879
- OpenAlex
- W2112837750
- Cited by
- 1,022
- References
- 40
- Citations by year
- 2026: 36 · 2025: 50 · 2024: 71 · 2023: 67 · 2022: 82 · 2021: 77 · 2020: 92 · 2019: 85 · 2018: 78 · 2017: 89 · 2016: 84 · 2015: 80 · 2014: 82 · 2013: 47 · 2012: 1
- FWCI
- 53.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (DP1OD003958)
- National Human Genome Research Institute (P01HG005062, P50HG006193)
- National Cancer Institute (DP1CA174427)
- National Institute of Allergy and Infectious Diseases (P01AI045757, P01AI073748, AI073748, AI045757)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK090105)
- National Institute of Neurological Disorders and Stroke (R01NS030843, R29NS030843, NS030843, NS045937, R37NS030843, R01NS045937)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- SGK1, Th17 cells, IL23R, high-salt diet, NFAT5, p38 MAPK, FOXO1, experimental autoimmune encephalomyelitis, autoimmunity, CD4+ T cells, IL-17, gene expression profiling, gene regulatory networks, salt intake, neuroinflammation, salt sensing
- MeSH terms
- Forkhead Box Protein O1, Serum-Glucocorticoid Regulated Kinases, Animals, Cell Differentiation, Encephalomyelitis, Autoimmune, Experimental, Humans, Interferon-gamma, Phenotype, Phosphorylation, Sodium Chloride, Protein Serine-Threonine Kinases, Sodium Chloride, Dietary, Immediate-Early Proteins, Receptors, Interleukin, Interleukin-17, Mice, Forkhead Transcription Factors, HEK293 Cells, Th17 Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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