FIGURE 1.

Schematic illustration of immune effector cell‐associated neurotoxicity syndrome (ICANS) pathogenesis after chimeric antigen receptor T‐cell (CAR‐T) treatment and potentially relevant management. After infusion of CAR‐T cell product into patients, CAR‐T cell is activated by engaging with tumor cell (not shown) and induces host myeloid cell activation. The interaction between CAR‐T cell and myeloid cell creates excessive circulating cytokines that contribute to endothelial activation‐induced blood–brain barrier (BBB) dysfunction. Increased permeability of BBB facilitates infiltration of peripheral immunocytes and cytokines into the central nervous system (CNS), which induces further CNS inflammation and abnormal neuronal function, together presenting typical symptoms of ICANS. Potentially relevant managements include key cytokines targeting, adhesion molecules blocking, and CAR‐T cell modulation to reduce immune effector cell‐associated neurotoxicity syndrome (ICANS) severity or prevent its occurrence.