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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Immunity 2018 ; 48 (3): 542-555.e6 Nephropedia Template TP
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Mitochondria?ER contact sites are immunometabolic hubs that orchestrate the rapid recall response of memory CD8+ T cells #MMPMID29523440
Bantug GR; Fischer MG; Grählert J; Balmer ML; Unterstab G; Develioglu L; Steiner R; Zhang L; da Costa ASH; Gubser PM; Burgener AV; Sauder U; Löliger J; Belle R; Dimeloe S; Lötscher J; Jauch A; Recher M; Hönger G; Hall MN; Romero P; Frezza C; Hess C
Immunity 2018[Mar]; 48 (3): 542-555.e6 PMID29523440show ga
Glycolysis is linked to the rapid recall capacity of memory CD8+ T cells, but the pathways that glucose fuels and the molecular and subcellular structural elements enabling enhanced glucose metabolism in nascent activated memory CD8+ T cells are not known. We found that mitochondria?ER contact sites are immunometabolic hubs that integrate mTORC2-initiated signaling with glucose metabolism and mitochondrial respiration in memory CD8+ T cells. Specifically, in this subcellular compartment, mTORC2, Akt and Gsk-3? were present by default. Rapid activation of Akt by mTORC2 led to inhibition of Gsk-3? at mitochondria?ER junctions, enabling recruitment of hexokinase I (HK-I) to the mitochondrial channel, VDAC. Binding of HK-I to VDAC promoted cellular respiration by facilitating metabolite flux into mitochondria. Glucose tracing pinpointed pyruvate oxidation in mitochondria, which was the metabolic requirement for rapid generation of IFN-? in memory T cells. Subcellular organization of key signaling events enabling HK-I recruitment to VDAC thus underpins the metabolic reprogramming needed for memory CD8+ T cells to rapidly acquire effector function.