Abstract
Immune checkpoint inhibitors (ICIs), exemplified by anti-PD-1 are promising treatments for many tumors. However, the majority of patients lack effective responses because of the emergence of immune-refractory tumors that disrupt the amplification of antitumor immunity. In many cases, one of the major causes of resistance to these agents is the limited tumor penetrance of effector T cells. Durable clinical responses using anti–PD-1 have been associated with T cell–inflamed tumor microenvironment (TME) favoring the infiltration of functional cytotoxic T lymphocytes (CTLs).
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