| First Author | Vaeth M | Year | 2017 |
| Journal | Immunity | Volume | 47 |
| Issue | 4 | Pages | 664-679.e6 |
| PubMed ID | 29030115 | Mgi Jnum | J:259234 |
| Mgi Id | MGI:6141288 | Doi | 10.1016/j.immuni.2017.09.003 |
| Citation | Vaeth M, et al. (2017) Store-Operated Ca(2+) Entry Controls Clonal Expansion of T Cells through Metabolic Reprogramming. Immunity 47(4):664-679.e6 |
| abstractText | Store-operated Ca(2+) entry (SOCE) is the main Ca(2+) influx pathway in lymphocytes and is essential for T cell function and adaptive immunity. SOCE is mediated by Ca(2+) release-activated Ca(2+) (CRAC) channels that are activated by stromal interaction molecule (STIM) 1 and STIM2. SOCE regulates many Ca(2+)-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 nutrient-sensing 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. |
