Figure 1.

Mechanism of ICIs associated pancreatic adverse events. Anti-PD-1/PD-L1 and anti-CTLA-4 monoclonal antibodies bind and block inhibitory signals, thus causing the widespread activation and expansion of T lymphocytes by blocking the inhibitory signals of T cells and enhancing the ability of the immune system to fight cancer cells. CD3+ T lymphocytes densely infiltrate the pancreatic islets, thereby increasing the ratio of CD8+/CD4+ T lymphocytes in peritumoral areas. The increased CD8+ T cells may cause damage to pancreatic cells, including islet β-cells and acinar, thereby destroying exocrine and endocrine pancreatic tissues which lead to a decrease in endocrine and exocrine pancreatic function. Meanwhile, a small proportion of patients would accompanied by peripancreatic fatty infiltration and pancreatic atrophy. APC, antigen-presenting cell; MHC, major histocompatibility complex; TCR, T cell receptor.