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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: Cancer Lett. 2017 Sep 1;408:190–196. doi: 10.1016/j.canlet.2017.08.033

Figure 1. Sensitivity to critical apoptosis pathways correlates with metabolic reprogramming over the course of the T cell response.

Figure 1

Naïve T cells exist in a metabolically quiescent state until antigen (Ag stimulation), which triggers increased Glut1-mediated glucose uptake and an abrupt increase in aerobic glycolysis (as well as OXPHOS). Enhanced glycolysis sensitizes effector T cells to RICD by enabling TCR-induced FASL induction upon Ag re-encounter. As Ag is cleared, most effector T cells are culled through CWID. Those T cells that persist into the memory pool likely escape both RICD and CWID by inducing protective autophagy and turning off glycolysis in favor of FAO-direct OXPHOS. This metabolic switch returns memory T cells to a more quiescent state, “primed” for rapid recall responses via increased spare respiratory capacity.