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. 2022 Mar 30;19(5):561–576. doi: 10.1038/s41423-022-00851-8

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — In monocytes/macrophages, high-salt enters proinflammatory cells via NCX1, causing NFAT5 expression and subsequent NO production by NOS2. In addition, proinflammatory cytokines such as IL-1β, IL-6, and TNF-α are released in response to high salt. In T cells, sodium enters the cell through the NKCC1 transporter, resulting in the upregulation of NFAT5 and its downstream target SGK1. Upregulation of the T_H17 transcription marker RORγt mediates the transcription and translation of IL-23R, which is essential for T_H17 induction and the secretion of IL-17a. NCX1 sodium calcium exchanger 1, NKCC1 sodium potassium chloride cotransporter, NOS2 nitric oxide synthase, NO nitric oxide, IL interleukin, TNF tumor necrosis factor, SGK1 serum glucocorticoid-regulated kinase, NFAT5 nuclear factor of activated T cells, RORγt retinoic-acid receptor-related orphan nuclear receptor gamma, M/M monocyte/macrophage