Sodium chloride, SGK1, and Th17 activation

Pflugers Arch. 2015 Mar;467(3):543-50. doi: 10.1007/s00424-014-1659-z. Epub 2014 Dec 4.

Abstract

The incidence of autoimmune diseases in Western civilizations is increasing rapidly, suggesting an influence of environmental factors, such as diet. The pathogenesis of several of these autoimmune diseases is characterized by aberrant activation of T helper 17 (Th17) cells. Recent reports have shown that the differentiation of Th17 cells is sensitive to changes in local microenvironments, in particular salt (NaCl) concentrations, in a molecular mechanism centered around the serum- and glucocorticoid-inducible kinase 1 (SGK1). In this review, we summarize the recently disclosed mechanisms by which salt has been shown to affect SGK1 and, subsequently, Th17 activation.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Immediate-Early Proteins / genetics
  • Immediate-Early Proteins / metabolism*
  • Lymphocyte Activation*
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Serine-Threonine Kinases / metabolism*
  • Sodium Chloride / metabolism*
  • Th17 Cells / immunology
  • Th17 Cells / metabolism*

Substances

  • Immediate-Early Proteins
  • Sodium Chloride
  • Protein-Serine-Threonine Kinases
  • serum-glucocorticoid regulated kinase