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Low oxygen tensions in the lung TME create hypoxia, activating HIF-1, which can paradoxically support T cell glycolysis but also induce exhaustion markers (e.g., PD-1, LAG-3) and compromise long-term memory formation

The activation of AMPK broadly suppresses proinflammatory signaling pathways, including the JAK-STAT, NF-B, C/EBP, CHOP, and HIF-1 pathways, which in turn inhibits the expansion and immunosuppressive function of myeloid-derived suppressor cells (MDSCs) 42

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Br J Cancer 91 : 17351741 She QB et al