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Lactylation significantly increases HMGB1 release from hepatocytes, a key component of damage-associated molecular patterns, actively mediating subsequent liver IRI

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This interaction modulates the equilibrium among Th1, Th2, Th17, Treg, and other T cell subsets, subsequently regulating inflammatory responses ( + T cell production of IL-2, correcting abnormal expression of IL-17A and IL-2, and benefiting CD4 + T cells in lupus prone mice and SLE patients ( Figure 3 )

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