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However, during chronic infection, Brucella circumvents these defenses by preferentially replicating in M2-like macrophages, where it benefits from increased glucose accumulation driven by the activity of peroxisome proliferator-activated receptor γ (PPARγ)

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Studies indicate that blocking glutamine metabolism in tumor cells can enhance the expression of PD-L1, enabling tumor cells to evade T cell-mediated immune killing (191, 192)