In addition, BMS-202 releasedin TME blocked PD-1/PD-L1 interaction to achieve ICB-based immunotherapy.As expected, Cele-BMS-NP treatment promoted tumor infiltration ofCD8+ Teff cells significantly and decreased intratumoralimmunosuppressive M2-like TAMs, Tregs, and PGE2, thus eliciting anefficient antitumor immunity to inhibit the growth of poorly immunogenic4T1 breast tumors. Here, PDCD1 is linked to neoplasm.