Apigenin modulates immune checkpoint molecules in pancreatic cancer enhancing anti-tumor immunity

• DOI: 10.4049/jimmunol.204.supp.241.17
• Publication Date: 2023-01-01T14:50:17Z
• Authors: Krystal Villalobo...; Jessica Luongo; Ari Marsh; Javier Areas; Bradley Miller; Tanika Williamson; Kazim Husain; Tomar Ghansah
• Keywords: Immune checkpoint

Abstract Pancreatic cancer (PC) remains as a very aggressive malignancy with an extremely poor prognosis and overall 5-year survival rate of only 8%. Immunotherapies are promising against solid tumors exception PC. This is partly due to PC’s inflammatory tumor microenvironment, resulting in increased expression both Programmed Death-Ligand (PD-L1) cell death protein 1 (PD-1) on effector CD8+ T cells. Upon PD-L1/PD-1 interaction, cells exhibit anergy, allowing PC evasion progression. We hypothesize that reducing PC-induced inflammation will increase anti-tumor immune responses promote regression. Therefore, we examined the checkpoint molecules (PD-L1, PD-L2, PD-1, Major Histocompatibility Complex-I, etc.) different murine lines (i.e. Panc02, UN-KPC-960, UN-KC-6141) modulation by anti-cancer natural bioflavonoid called apigenin (API). To do this, treated lines, vitro, without API along interferon-γ (potent inducer PD-L1) detect profiles these using flow cytometry. Subsequently, tested proliferation response untreated/treated Our results show down-regulated PD-L1 which coincides responses. suggest may reduce immunosuppression immunity. clinical application adjuvant potentiate efficacy current immunotherapies.