Two recent publications suggest that dietary salt may polarize TH17 cells and therefore increase the risk of developing autoimmune disease. Where low salt diets can readily be tested for their therapeutic effects in autoimmune disease, more work is needed to connect dietary salts with the development of immunopathology.

Sodium represents the most abundant cation in the extracellular fluid, where it performs a plethora of biological processes ranging from establishment of cellular membrane potential to osmotic balance. Although sodium is an essential nutrient, in recent years the intake of sodium derived from salt-rich diets across the globe has dramatically increased with numerous detrimental effects being projected including cardiovascular complications and hypertension [1]. Two recent publications postulate a new set of dangers associated with this alarming trend, and hypothesize that rising dietary salt intake may represent a long sought-after link to the ever-increasing prevalence of autoimmunity in the developed world [2, 3]. Both publications outline a mechanism by which increased salt in our diets can render T cells more receptive to IL-23 signaling, a cytokine historically linked to a number of autoimmune diseases including multiple sclerosis (MS), inflammatory bowel disease (IBD), rheumatoid arthritis (RA) and psoriasis. IL-23 is a cytokine like few others, in that its requirement for induction of proinflammatory autoimmune disease states in animal models is seemingly absolute [4]. Both manuscripts describe a role of the serum glucocorticoid kinase