Nalecz Institute of Biocybernetics and Biomedical Engineering Polish Academy of Sciences, 02-109 Warsaw, Poland.
Int J Mol Sci. 2023 Jun 13;24(12):10068. doi: 10.3390/ijms241210068.
Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of solid malignancies, including non-small-cell lung cancer. However, immunotherapy resistance constitutes a significant challenge. To investigate carbonic anhydrase IX (CAIX) as a driver of resistance, we built a differential equation model of tumor-immune interactions. The model considers treatment with the small molecule CAIX inhibitor SLC-0111 in combination with ICIs. Numerical simulations showed that, given an efficient immune response, CAIX KO tumors tended toward tumor elimination in contrast to their CAIX-expressing counterparts, which stabilized close to the positive equilibrium. Importantly, we demonstrated that short-term combination therapy with a CAIX inhibitor and immunotherapy could shift the asymptotic behavior of the original model from stable disease to tumor eradication. Finally, we calibrated the model with data from murine experiments on CAIX suppression and combination therapy with anti-PD-1 and anti-CTLA-4. Concluding, we have developed a model that reproduces experimental findings and enables the investigation of combination therapies. Our model suggests that transient CAIX inhibition may induce tumor regression, given a sufficient immune infiltrate in the tumor, which can be boosted with ICIs.
免疫检查点抑制剂 (ICIs) 彻底改变了实体恶性肿瘤的治疗方法,包括非小细胞肺癌。然而,免疫治疗耐药性是一个重大挑战。为了研究碳酸酐酶 IX (CAIX) 作为耐药性的驱动因素,我们构建了一个肿瘤免疫相互作用的微分方程模型。该模型考虑了小分子 CAIX 抑制剂 SLC-0111 与 ICI 的联合治疗。数值模拟表明,在有效的免疫反应下,CAIX KO 肿瘤倾向于消除肿瘤,而 CAIX 表达的肿瘤则稳定在正平衡点附近。重要的是,我们证明了 CAIX 抑制剂与免疫治疗的短期联合治疗可以将原始模型的渐近行为从稳定疾病转变为肿瘤消除。最后,我们使用 CAIX 抑制和抗 PD-1 与抗 CTLA-4 联合治疗的小鼠实验数据对模型进行了校准。总之,我们开发了一个可以重现实验结果并能够研究联合治疗的模型。我们的模型表明,在肿瘤中有足够的免疫浸润的情况下,短暂的 CAIX 抑制可能会诱导肿瘤消退,而 ICI 可以增强这种免疫浸润。