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Emerging evidence suggests that changes in the environment and diet may contribute to disease. Experimental studies have demonstrated that excessive salt intake can modulate immune function by inducing pathogenic pro\u2010inflammatory T helper 17 cells (Th17) and impairing anti\u2010inflammatory regulatory T cell (Treg) function both in vitro and in vivo, thereby promoting autoimmunity. Serum\/glucocorticoid\u2010regulated kinase 1 (SGK1) has been identified as a central mediator of immune function in response to high salt. Additionally, alterations in immunometabolism and epigenetic modulations have been linked to immune dysfunction under high\u2010sodium conditions. Understanding the complex interplay between inflammatory processes, immunometabolism, and epigenetic regulation is essential for deciphering how ionic disturbances may shape T cell immunity and disease. 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