Dose-dependent enhancement of T-lymphocyte priming and CTL lysis following ionizing radiation in an engineered model of oral cancer

While many patients with head and neck squamous cell carcinoma (HNSCC) display a T-cell inflamed phenotype [1], only a small subset respond to programmed death (PD) pathway checkpoint inhibition [2]. Strategies to enhance response rates to checkpoint inhibition in HNSCC are needed. PD-based checkpoint blockade has the potential to unleash an existing anti-tumor immune response being blocked by the expression of PD-1/PD-L1, but cannot induce a de novo anti-tumor immunity [3]. The addition of PD-based checkpoint blockade to other anti-cancer treatments that have the potential to induce adaptive anti-tumor immune responses may be additive or synergistic due to reversal of adaptive immune resistance [3,4].

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