Several environmental factors are thought to contribute to the increasing incidence of autoimmune disease; however, it remains to be seen whether these factors directly influence immune cell development. Two new studies now reveal that increased dietary salt intake can promote autoimmune inflammation and the development of pathogenic T helper 17 (TH17) cells (Nature http://dx.doi.org/10.1038/nature11868 and http://dx.doi.org/10.1038/nature11984).
Kleinewietfeld et al. and Wu et al. reported that a mouse model of multiple sclerosis develops more severe disease when fed a high-salt diet. In vitro, an increased concentration of NaCl promotes the differentiation of both mouse and human TH17 cells. Mechanistically, NaCl induces the expression of serum glucocorticoid kinase 1 (SGK1). This kinase increases the expression of the IL-23 receptor, thereby stabilizing TH17 cells and promoting IL-17 secretion. Mice deficient in SGK1 develop attenuated disease, have fewer TH17 cells and are relatively resistant to the effects of high-salt diet on autoimmune inflammation.
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