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Genetic depletion of HIF-1 in T cells enhances oxidative metabolism and Treg output while suppressing Th17 responses, confirming its pivotal role in metabolic reprogramming ( The interplay between these regulators creates a dynamic checkpoint: mTORC1 and HIF-1 synergize to propel effector T cell responses under nutrient-rich conditions, whereas AMPK activation restrains anabolic metabolism to favor regulatory phenotypes during energy stress