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Targeting this metabolic heterogeneity through the inhibition of glycolytic enzymes (PFKFB3 via PFK15), upstream signaling molecules (mTORC1 via rapamycin), and transcription factors (HIF-1α/c-Myc via metformin) impairs pathogenic T cell responses by inducing functional exhaustion in CD4⁺ T cells, enhancing Treg suppressive function, and suppressing Th1 and Th17 differentiation