Fig. 2

The interplay of PANoptosis between cancer cells and TIME. On the one hand, PANoptotic tumor cells release inflammatory factors or DAMPs, which enhance DCs maturation, M2-to-M1 macrophage repolarization, CD4⁺/CD8⁺ T cell infiltration and activate NK cells, while deplete Tregs to orchestrate immune activation and subsequently suppress tumor development. On the other hand, macrophages are induced to PANoptosis via TNF-α + IFN-γ—JAK/STAT1—IRF1—RIPK1/caspase-8 axis, IFNs+NEIs—ADAR1—ZBP1 axis, or baicalin—mitochondrial injury—ZBP1 axis to enhance inflammatory responses and immune activation (CBL0137 is the agonist of ZBP1), while neutrophils are induced to PANoptosis via diABZI—STING—AIM2/NLRP3 axis and the interaction of GATA2—HMGB1—TIM-3 axis with DCs to inhibit immune activation