HE4 drives PD-L1 expression in myeloid cells via IFN-γR-JAK-STAT3 signaling to promote tumor immune evasion

T cell activity, and suppressed tumor growth in syngeneic and humanized models, while inducing fewer irAEs than PD-1 blockade. Clinically, high HE4 expression predicts poor prognosis but correlates with improved response to PD-1 inhibitors in lung adenocarcinoma, highlighting HE4 as both a therapeutic target and predictive biomarker.