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Figure 11: Mechanism by which a high-salt diet enhances the differentiation of naïve CD4+ cells to pathogenic TH17 cells that may exacerbate experimental autoimmune encephalitis. High salt concentration, change in osmolarity, the influence of IL-23 and IL-23 receptor signaling, and the activation of various enzymes drive the expression of TH17-associated cytokines and the formation of pathogenic TH17 phenotype.