Metabolites such as HMGB1 and glutamate released by dead cells can reshape the immune microenvironment through a dual mechanism (153): HMGB1 binds to TLR4 on the surface of DCs, activates the NF-κB pathway to promote DC maturation and MHC molecule expression, and then activates tumor antigen-specific CD8+ T cells; glutamate indirectly promotes DC migration by regulating metabolic balance, and directly recruits tumor-reactive T cells as a chemokine factor, ultimately shifting the ratio of effector T cells/regulatory T cells in the tumor microenvironment towards the pro-inflammatory direction. The gene discussed is TLR4; the disease is neoplasm.