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Graphical model of Glut1 blockade approach in patients with T1D undergoing to islet transplantation. Resting memory clones are activated by islet transplantation and rapidly increase glucose uptake via Glut1 to fuel glycolysis necessary for expansion, proliferation, and effector functions. Treatment with the Glut1 inhibitor WZB117 prevents metabolic re-programming to glycolysis and failure to fulfill bio-energetic needs drive T cells in a state of anergy and exhaustion.
