Both NK cells and ILC3 expressed functional PD-1, moreover, both tumor samples and malignant PE-derived tumor cell lines were PD-L1<sup>+</sup> suggesting that the interaction between PD-1<sup>+</sup> ILC and PD-L1<sup>+</sup> tumor cells may hamper antitumor immune responses mediated by NK and ILC.
We found that infiltrating T lymphocytes in PE manifest a more exhausted phenotype during αPD-1 therapy than during treatment with other cancer drugs, with subpopulations of these cells characterized by specific immune checkpoint protein and cytokine expression profiles possibly contributing to the antitumor immune response.