CD274 and neoplasm: Of note, increased PD-1/PD-L1 interactions in TDLN were identified as restraining antitumor T-cell immunity through increased PD-L1 levels on tumor-conditioned DCs (7); PD-L1 blockade resulted in DC-mediated expansion of progenitor-exhausted T cells, which, upon making their way to the tumor, could expand, and differentiate further to mediate antitumor effector functions.