SGK1 is a serine-threonine kinase that plays a critical role in the induction of pathogenic Th17 cells. Th17 cells are proinflammatory and essential for clearing extracellular pathogens but also contribute to autoimmune diseases. IL-23 is crucial for maintaining Th17 phenotype by increasing IL-23R expression and promoting pathogenic effector functions. However, the molecular mechanism by which IL-23 sustains Th17 response and induces pathogenic functions remains unclear. This study identifies SGK1 as a key node downstream of IL-23 signaling that regulates IL-23R expression and stabilizes Th17 cells by deactivating Foxo1, a repressor of IL-23R. SGK1 is also involved in Na+ transport and salt homeostasis. A modest increase in salt concentration induces SGK1 expression, promoting IL-23R expression and enhancing Th17 differentiation in vitro and in vivo, accelerating autoimmunity. Loss of SGK1 abrogates Na+-mediated Th17 differentiation in an IL-23-dependent manner. These findings demonstrate that SGK1 is essential for Th17 induction and provide insight into how environmental factors like high salt diets can trigger Th17 development and promote tissue inflammation. The study used transcriptional profiling of developing Th17 cells to construct a signaling network and identify key regulators. SGK1 was found to be highly expressed during Th17 differentiation and its expression is specifically induced by IL-23. SGK1-deficient Th17 cells showed impaired IL-17 production upon restimulation with IL-23. Network analysis of transcriptional changes in IL-23R-deficient T cells identified SGK1 as a potential nodal point downstream of IL-23R signaling. SGK1 was shown to phosphorylate Foxo1, leading to its deactivation and promoting RORγt-mediated IL-23R expression. SGK1-deficient mice exhibited reduced EAE incidence and severity, with reduced IL-17 production from infiltrating CD4+ T cells. These findings support a model where SGK1's effect on Foxo1 phosphorylation is a key step in relieving RORγt from Foxo1-mediated inhibition, enhancing IL-23R expression. SGK1 is also involved in Na+ homeostasis and its expression is induced by NaCl. In vivo, a high salt diet increased Th17 cell frequency in the gut and gut-associated lymphoid tissue, with SGK1-deficient mice showing a milder enhancement. Mice fed a high salt diet showed increased EAE severity, which was reduced in SGK1-deficient mice. These results indicate that high sodium intake potentiates Th17 cell generation in an SGK1-dependent manner, potentially increasing the risk of promoting autoimmunity. The study highlights the roleSGK1 is a serine-threonine kinase that plays a critical role in the induction of pathogenic Th17 cells. Th17 cells are proinflammatory and essential for clearing extracellular pathogens but also contribute to autoimmune diseases. IL-23 is crucial for maintaining Th17 phenotype by increasing IL-23R expression and promoting pathogenic effector functions. However, the molecular mechanism by which IL-23 sustains Th17 response and induces pathogenic functions remains unclear. This study identifies SGK1 as a key node downstream of IL-23 signaling that regulates IL-23R expression and stabilizes Th17 cells by deactivating Foxo1, a repressor of IL-23R. SGK1 is also involved in Na+ transport and salt homeostasis. A modest increase in salt concentration induces SGK1 expression, promoting IL-23R expression and enhancing Th17 differentiation in vitro and in vivo, accelerating autoimmunity. Loss of SGK1 abrogates Na+-mediated Th17 differentiation in an IL-23-dependent manner. These findings demonstrate that SGK1 is essential for Th17 induction and provide insight into how environmental factors like high salt diets can trigger Th17 development and promote tissue inflammation. The study used transcriptional profiling of developing Th17 cells to construct a signaling network and identify key regulators. SGK1 was found to be highly expressed during Th17 differentiation and its expression is specifically induced by IL-23. SGK1-deficient Th17 cells showed impaired IL-17 production upon restimulation with IL-23. Network analysis of transcriptional changes in IL-23R-deficient T cells identified SGK1 as a potential nodal point downstream of IL-23R signaling. SGK1 was shown to phosphorylate Foxo1, leading to its deactivation and promoting RORγt-mediated IL-23R expression. SGK1-deficient mice exhibited reduced EAE incidence and severity, with reduced IL-17 production from infiltrating CD4+ T cells. These findings support a model where SGK1's effect on Foxo1 phosphorylation is a key step in relieving RORγt from Foxo1-mediated inhibition, enhancing IL-23R expression. SGK1 is also involved in Na+ homeostasis and its expression is induced by NaCl. In vivo, a high salt diet increased Th17 cell frequency in the gut and gut-associated lymphoid tissue, with SGK1-deficient mice showing a milder enhancement. Mice fed a high salt diet showed increased EAE severity, which was reduced in SGK1-deficient mice. These results indicate that high sodium intake potentiates Th17 cell generation in an SGK1-dependent manner, potentially increasing the risk of promoting autoimmunity. The study highlights the role