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data was processed using the genepattern suite . differentially expressed genes were detected using fold - change and t - test analysis ( for sgk1 and nacl - treated t cells ) , a consensus of fold - change , the edge software and a novel sigmoid - based method ( for the il23r th17 cell time course data ) .
nave t cells were facs - sorted , stimulated with plate bound anti - cd3/cd28 and the indicated cytokines or nacl and cells were analyzed by qpcr or flow cytometry at different time points .
mice were immunized subcutaneously with mog3555 , cfa , heat - inactivated mycobacterium tuberculosis and with intraperitoneal injection of bordatella pertussis toxin .
nave t cells were differentiated towards th17 cells , then transferred into mog3555/cfa immunized hosts and t cells isolated from various organs were analyzed by flow cytometry at 712 days after onset of eae . differentiated t cells or transfected hek293 t cells were lysed in wce buffer and
lysates were subjected to western blot or immunoprecipitation analysis . hek 293 t cells were transfected with luciferase reporter constructs and expression vectors and luciferase expression was determined after 48 h.
data was processed using the genepattern suite . differentially expressed genes were detected using fold - change and t - test analysis ( for sgk1 and nacl - treated t cells ) , a consensus of fold - change , the edge software and a novel sigmoid - based method ( for the il23r th17 cell time course data ) .
nave t cells were facs - sorted , stimulated with plate bound anti - cd3/cd28 and the indicated cytokines or nacl and cells were analyzed by qpcr or flow cytometry at different time points .
mice were immunized subcutaneously with mog3555 , cfa , heat - inactivated mycobacterium tuberculosis and with intraperitoneal injection of bordatella pertussis toxin .
nave t cells were differentiated towards th17 cells , then transferred into mog3555/cfa immunized hosts and t cells isolated from various organs were analyzed by flow cytometry at 712 days after onset of eae .
differentiated t cells or transfected hek293 t cells were lysed in wce buffer and lysates were subjected to western blot or immunoprecipitation analysis .
hek 293 t cells were transfected with luciferase reporter constructs and expression vectors and luciferase expression was determined after 48 h.
th17 cells are highly proinflammatory cells critical for clearing extracellular pathogens and for induction of multiple autoimmune diseases1 . 
 il-23 plays a critical role in stabilizing and reinforcing the th17 phenotype by increasing expression of il-23 receptor ( il-23r ) and endowing th17 cells with pathogenic effector functions2 , 3 . 
 however , the precise molecular mechanism by which il-23 sustains the th17 response and induces pathogenic effector functions has not been elucidated . here , we used transcriptional profiling of developing th17 cells to construct a model of their signaling network and nominate major nodes that regulate th17 development . 
 we identified serum glucocorticoid kinase-1 ( sgk1 ) , a serine - threonine kinase4 , as an essential node downstream of il-23 signaling . 
 sgk1 is critical for regulating il-23r expression and stabilizing the th17 cell phenotype by deactivation of foxo1 , a direct repressor of il-23r expression . 
 sgk1 has been shown to govern na+ transport and salt ( nacl ) homeostasis in other cells5 , 6 , 7 , 8 . 
 we here show that a modest increase in salt concentration induces sgk1 expression , promotes il-23r expression and enhances th17 cell differentiation in vitro and in vivo , accelerating the development of autoimmunity . 
 loss of sgk1 abrogated na+-mediated th17 differentiation in an il-23-dependent manner . 
 these data demonstrate that sgk1 plays a critical role in the induction of pathogenic th17 cells and provides a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers th17 development and promotes tissue inflammation .