Abstract 7129: PDL1 expression on immune cells from solid tumor patients: Implications for tumor immunity and immunotherapy

Abstract Programmed death-ligand 1 (PD-L1) is a key immune checkpoint molecule that regulates immune responses by binding to PD-1 on T cells, contributing to immune tolerance and suppression. PD-L1 expression in solid tumors has become an important biomarker for evaluating the efficacy of immune checkpoint inhibitors in cancer therapy. Characterization of PD-L1 expression on immune cells, particularly CD8+ T cells, in patients with various solid tumors, including melanoma, non-small cell lung cancer (NSCLC), and breast cancer was performed using cryopreserved peripheral blood mononuclear samples using flow cytometry. In addition to PD-L1, co-expression of markers of T cell activation (e.g., CD69, CD86, Ki67) and exhaustion (e.g., PD-1, LAG3) was analyzed to gain a comprehensive understanding of immune cell status. PD-L1 expression was highly variable across patients within solid tumor indications, with elevated expression found on CD8+ T cells, suggesting an upregulation in response to persistent tumor antigenic stimulation. Furthermore, PD-L1+ CD8+ T cells often co-expressed markers of exhaustion, such as PD-1 and LAG-3, indicating a potential role for PD-L1 in T cell dysfunction and immune evasion. These findings underscore the complexity of PD-L1 expression by immune cells and its role in shaping immune responses in solid tumor patients. Through integrating PD-L1 profiling with other markers of immune activation and exhaustion, this highlights the potential of PD-L1 as a predictive biomarker for immunotherapy response and provides insights into the mechanisms of immune evasion in solid tumor cancers. Citation Format: Angelina Bisconte, Rachel Owen, Jackie Benko, Jorge Pardo, Samantha Splitt, Deb Phippard. PDL1 expression on immune cells from solid tumor patients: Implications for tumor immunity and immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 7129.