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Although the underlying mechanism involved in the upregulation of PD-1 remains to be explored, it has recently been implicated that in chronic LCMV infection mice, T-bet represses expression of PD-1 and sustains exhausted CD8 + T cells

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Immune cells typically utilize OXPHOS as their primary energy source when quiescent, but stimulation from Toll-like receptors (TLRs) or proinflammatory cytokines can induce metabolic reprogramming to support activation and downstream effector functions [19,20]

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