Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Department of Translational Science, Nanobiotix, Paris, France.
Front Immunol. 2022 Nov 3;13:1022011. doi: 10.3389/fimmu.2022.1022011. eCollection 2022.
The efficacy of immunoradiotherapy consisting of radiation therapy and immune checkpoint blockade relies on effectively promoting the systemic antitumor immune response's activation while simultaneously reducing local factors favoring immune suppression. We previously demonstrated that NBTXR3, a nanoparticle radioenhancer, significantly improved immune responses in a murine anti-PD1-resistant metastatic lung cancer model. We hypothesize that radioactivated-NBTXR3 addition to anti-PD1 and a second-generation anti-CTLA4 could improve treatment effectiveness. To test this hypothesis, we inoculated mice with 344SQR cells in the right and left legs to establish primary and secondary tumors. The primary tumors were intratumorally injected with NBTXR3 nanoparticles on day 7, followed by three fractions of 12 Gy radiation on days 8, 9, and 10. The secondary tumors received two fractions of 1Gy radiation on days 13 and 14. Multiple rounds of anti-PD1, anti-CTLA4 or nonfucosylated anti-CTLA4 were given to the mice. Immune profiling of the tumors revealed that the combination of NBTXR3 with immunoradiotherapy significantly upregulated the activities of a wide range of antitumor immune pathways and reduced the abundance of regulatory suppressor T cells. This combination effectively eradicated the primary and secondary tumors and increased animal survival to 75%. Remarkably, previously treated with NBTXR3-containing treatment, the survivor mice exhibited a long-lasting antitumor memory immune response. This data provides compelling evidence of the efficacy of NBTXR3 to synergize with the immunoradiotherapy approach when combined with an anti-PD1 and multiple checkpoints such as a second generation anti-CTLA4 and show the potential for clinical uses of antitumor immunomodulatory effects of NBTXR3.
免疫放疗的疗效依赖于有效地促进全身抗肿瘤免疫反应的激活,同时减少有利于免疫抑制的局部因素。我们之前证明,纳米颗粒放射增敏剂 NBTXR3 可显著改善抗 PD-1 耐药转移性肺癌模型中的免疫反应。我们假设,放射性激活的 NBTXR3 联合抗 PD-1 和第二代抗 CTLA4 可以提高治疗效果。为了验证这一假设,我们将 344SQR 细胞接种到小鼠的右后腿和左后腿中,以建立原发性和继发性肿瘤。原发性肿瘤在第 7 天经瘤内注射 NBTXR3 纳米颗粒,随后在第 8、9 和 10 天接受 3 次 12 Gy 的分次照射。继发性肿瘤在第 13 和 14 天接受 2 次 1Gy 的分次照射。多次给予小鼠抗 PD-1、抗 CTLA4 或非岩藻糖基化抗 CTLA4。对肿瘤进行免疫分析表明,NBTXR3 与免疫放疗联合使用可显著上调多种抗肿瘤免疫途径的活性,并减少调节性抑制性 T 细胞的丰度。这种联合治疗有效地根除了原发性和继发性肿瘤,使动物的存活率提高到 75%。值得注意的是,先前接受过含 NBTXR3 治疗的幸存者小鼠表现出持久的抗肿瘤记忆免疫反应。这些数据有力地证明了 NBTXR3 与免疫放疗联合使用时与抗 PD-1 和多种检查点(如第二代抗 CTLA4)联合使用的疗效,并显示了 NBTXR3 抗肿瘤免疫调节作用的临床应用潜力。