Sodium chloride, SGK1, and Th17 activation

被引：41
作者：
Binger, Katrina J. [1 ]
Linker, Ralf A. [2 ]
Muller, Dominik N. [1 ,3 ]
Kleinewietfeld, Markus [4 ]
机构：
[1] Expt & Clin Res Ctr, D-13125 Berlin, Germany
[2] Univ Erlangen Nurnberg, D-91054 Erlangen, Germany
[3] Max Delbruck Ctr Mol Med, D-13125 Berlin, Germany
[4] Tech Univ Dresden, Med Fac Carl Gustav Carus, D-01307 Dresden, Germany
来源：
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY | 2015年 / 467卷 / 03期
关键词：
Salt; SGK1; T cells; Autoimmunity; PATHOGENIC T(H)17 CELLS; INDUCIBLE KINASE SGK; T-HELPER; 17; NF-KAPPA-B; REGULATORY T; TRANSCRIPTION FACTORS; AUTOIMMUNE-DISEASE; BLOOD-PRESSURE; UP-REGULATION; TGF-BETA;
D O I：
10.1007/s00424-014-1659-z
中图分类号：
Q4 [生理学];
学科分类号：
071003 ;
摘要：
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.
引用
收藏
页码：543 / 550
页数：8
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