Figure 1. Immune checkpoint inhibition unleashes T cell responses and drives T cell- and cytokine-mediated dermatotoxicity.

CTLA-4 inhibition enhances antigen-specific T cell priming, whereas PD-1 inhibition repositions T cells for antigen access and unlocks their effector potential. CTLA-4 and PD-1 inhibitor treatment causes cutaneous adverse events by mobilizing T cells reactive to self-antigens and commensal bacterial antigens.