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Validation in mouse models of MPP suggests that the CXCL12/CXCR4 axis activates both JAK-STAT and NF-B pathways to exert synergistic proinflammatory effects, making it a key therapeutic target for MPP (131)

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However, as CD8+ T cells differentiate to effector cells, loss of HIF-1 impairs expression of genes controlling glycolysis and glycolytic capacity, albeit not completely (Finlay et al., 2012)