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This may result from tumor-mediated glucose restriction, which limits T-cell substrate availability and suppresses mTOR activity, glycolysis, and IFN- production, thereby promoting functional exhaustion while promoting tumor progression [171]

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Dauer W, Kholodilov N, Vila M, Trillat AC, Goodchild R, Larsen KE, Staal R, Tieu K, Schmitz Y, Yuan CA, Rocha M, Jackson-Lewis V, Hersch S, Sulzer D, Przedborski S, Burke R, Hen R, 2002