Fig. 1

The potential mechanism of irAE related to ICI treatment. A Blocking CTLA-4 can induce the activation of autoreactive T cells by inducing Treg depletion and functional defects, thereby stimulating B cells to increase the production of autoantibodies. B Blocking CTLA4 and/or PD1 may be related to the expansion and activation of pre-existing tissue-resident memory T cells. C Blocking PD-1 can induce the reactivation of depleted/disabled T cells, which leads to the overactivation of autoreactive T cells. Epitope diffusion can lead to the destruction of tolerance. D The death of tumor cells killed by T cells can induce an increase in the level of pro-inflammatory cytokines, which in turn leads to damage to normal tissues or organs. E ICl may directly damage tissues or organs by binding to CTLA-4 and/or PD1 expressed in normal tissues. DC, dendritic cells; MHC, major histocompatibility complex; Treg, regulatory T cells; TCR, T cell receptor