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Sodium chloride is an ionic checkpoint for human TH2 cells and shapes the atopic skin microenvironment.

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Affiliations

  • 1. Institute of Virology, Technical University of Munich, 81675 Munich, Germany.
      Authors
    • Matthias J 1, 3, 7
    • Meinl H 1, 7
    • Chao YY 1, 7
    • Soll D 1, 7
    • Zielinski CE 1, 3, 7
    (5 authors)
  • 2. Institute for Immunology, Biomedical Center, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
      Authors
    • Maul J 2
    • Baumjohann D 2
    (2 authors)
  • 3. Department of Dermatology, Unit Cellular Immunoregulation, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
      Authors
    • Matthias J 1, 3, 7
    • Noster R 3
    • Zielinski CE 1, 3, 7
    (3 authors)
  • 4. ZWE FRM II, Technical University of Munich, 85748 Garching, Germany.
      Authors
    • Gerstenberg H 4
    • Jeschke F 4
    (2 authors)
  • 5. Department of Genetics, University of Saarland, 66123 Saarbrücken, Germany.
      Authors
    • Gasparoni G 5
    • Welle A 5
    • Walter J 5
    • Nordström K 5
    (4 authors)
    • Show all (9)

ORCIDs linked to this article

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Science Translational Medicine, 01 Feb 2019, 11(480):eaau0683
https://doi.org/10.1126/scitranslmed.aau0683 PMID: 30787167 

This article is based on a previously available preprint.

Abstract 

The incidence of allergic diseases has increased over the past 50 years, likely due to environmental factors. However, the nature of these factors and the mode of action by which they induce the type 2 immune deviation characteristic of atopic diseases remain unclear. It has previously been reported that dietary sodium chloride promotes the polarization of T helper 17 (TH17) cells with implications for autoimmune diseases such as multiple sclerosis. Here, we demonstrate that sodium chloride also potently promotes TH2 cell responses on multiple regulatory levels. Sodium chloride enhanced interleukin-4 (IL-4) and IL-13 production while suppressing interferon-γ (IFN-γ) production in memory T cells. It diverted alternative T cell fates into the TH2 cell phenotype and also induced de novo TH2 cell polarization from naïve T cell precursors. Mechanistically, sodium chloride exerted its effects via the osmosensitive transcription factor NFAT5 and the kinase SGK-1, which regulated TH2 signature cytokines and master transcription factors in hyperosmolar salt conditions. The skin of patients suffering from atopic dermatitis contained elevated sodium compared to nonlesional atopic and healthy skin. These results suggest that sodium chloride represents a so far overlooked cutaneous microenvironmental checkpoint in atopic dermatitis that can induce TH2 cell responses, the orchestrators of atopic diseases.

Full text links 

Read article at publisher's site: https://doi.org/10.1126/scitranslmed.aau0683

Read article for free, from open access legal sources, via Unpaywall: https://stm.sciencemag.org/content/scitransmed/11/480/eaau0683.full.pdfUnpaywall

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Funding 

Funders who supported this work.

DFG (1)

Deutsche Forschungsgemeinschaft (3)

Fritz Thyssen Stiftung

    German Center for Infection Research