期刊
IMMUNITY
卷 47, 期 4, 页码 664-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2017.09.003
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资金
- NIH SIG grant [1S10OD016304-01]
- NIH grant [AI097302]
- Department of Defense grant [W81XWH-15-1-0337]
- Deutsche Forschungsgemeinschaft (DFG) [TRR52, SE 469/22-1]
- DFG postdoctoral fellowship [VA 882/1-1]
- Wilhelm Sander Foundation [2010.095.1-3]
- Alex Lemonade Stand Foundation
Store-operated Ca2+ entry (SOCE) is the main Ca2+ influx pathway in lymphocytes and is essential for T cell function and adaptive immunity. SOCE is mediated by Ca2+ release-activated Ca2+ (CRAC) channels that are activated by stromal interaction molecule (STIM) 1 and STIM2. SOCE regulates many Ca2+-dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impairs antigen-dependent T cell proliferation. We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cells by controlling glycolysis and oxidative phosphorylation. SOCE directs the metabolic reprogramming of naive T cells by regulating the expression of glucose transporters, glycolytic enzymes, and metabolic regulators through the activation of nuclear factor of activated T cells (NFAT) and the PI3K-AKT kinase-mTOR nutrientsensing pathway. We propose that SOCE controls a critical metabolic checkpoint'' at which T cells assess adequate nutrient supply to support clonal expansion and adaptive immune responses.
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