ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation

Conclusions: ILT4 was induced by activation of EGFR-AKT and ERK1/2 signaling in NSCLC cells. Overexpressed ILT4 suppressed tumor immunity by recruiting M2-like TAMs and impairing T cell response, while ILT4 inhibition prevented immunosuppression and tumor promotion. Furthermore, ILT4 inhibition enhanced the efficacy of PD-L1 inhibitor in EGFR wild-type but not in EGFR mutant NSCLC. Our study identified novel mechanisms for EGFR-mediated tumor immune escape, and provided promising immunotherapeutic strategies for patients with EGFR-activated NSCLC.

Source: Theranostics - April 19, 2021 Category: Molecular Biology Authors: Xiaozheng Chen, Aiqin Gao, Fang Zhang, Zijiang Yang, Shuyun Wang, Yuying Fang, Juan Li, Jingnan Wang, Wenjing Shi, Linlin Wang, Yan Zheng, Yuping Sun Tags: Research Paper Source Type: research