A study published in Nature (2013) reveals that high sodium chloride (NaCl) levels promote the development of pathogenic Th17 cells, which are involved in autoimmune diseases. The research shows that increased salt concentrations in the body enhance the induction of Th17 cells, which produce pro-inflammatory cytokines like IL-17A, TNF-α, and IL-2. These cells contribute to the progression of autoimmune diseases such as multiple sclerosis (MS) and type 1 diabetes. The study demonstrates that high-salt conditions activate the p38/MAPK pathway, involving TonEBP/NFAT5 and SGK1, leading to the generation of highly pathogenic Th17 cells. These cells are characterized by increased expression of pro-inflammatory cytokines and are associated with more severe forms of experimental autoimmune encephalomyelitis (EAE), an animal model for MS. The findings suggest that dietary salt intake may be an environmental risk factor for autoimmune diseases by inducing pathogenic Th17 cells. The study also highlights the role of the p38/MAPK, NFAT5, and SGK1 pathways in this process. The research underscores the potential of these pathways as therapeutic targets for autoimmune diseases.A study published in Nature (2013) reveals that high sodium chloride (NaCl) levels promote the development of pathogenic Th17 cells, which are involved in autoimmune diseases. The research shows that increased salt concentrations in the body enhance the induction of Th17 cells, which produce pro-inflammatory cytokines like IL-17A, TNF-α, and IL-2. These cells contribute to the progression of autoimmune diseases such as multiple sclerosis (MS) and type 1 diabetes. The study demonstrates that high-salt conditions activate the p38/MAPK pathway, involving TonEBP/NFAT5 and SGK1, leading to the generation of highly pathogenic Th17 cells. These cells are characterized by increased expression of pro-inflammatory cytokines and are associated with more severe forms of experimental autoimmune encephalomyelitis (EAE), an animal model for MS. The findings suggest that dietary salt intake may be an environmental risk factor for autoimmune diseases by inducing pathogenic Th17 cells. The study also highlights the role of the p38/MAPK, NFAT5, and SGK1 pathways in this process. The research underscores the potential of these pathways as therapeutic targets for autoimmune diseases.