Brüßeler Melanie M T, Zam Alaa, Moreno-Zafra Víctor M, Rouatbi Nadia, Hassuneh Osama W M, Marrocu Alessia, Liam-Or Revadee, Abdel-Bar Hend Mohamed, Walters Adam Alexander, Al-Jamal Khuloud T
Institute of Pharmaceutical Science, King's College London, Franklin-Wilkins Building 150 Stamford Street, London SE1 9NH, U.K.
Ludwig Maximilians University, Bayern, Munich, München 80539, Germany.
Mol Pharm. 2024 Dec 2;21(12):6339-6352. doi: 10.1021/acs.molpharmaceut.4c00875. Epub 2024 Nov 18.
Glioblastoma (GBM) immunotherapy is particularly challenging due to the pro-tumorigenic microenvironment, marked by low levels and inactive immune cells. Toll-like receptor (TLR) agonists have emerged as potent immune adjuvants but failed to show improved outcomes in clinical trials when administered as a monotherapy. We hypothesize that a combined nanoparticulate formulation of TLR agonist and immunogenic cell death-inducing drug (doxorubicin) will synergize to induce improved GBM immunotherapy. Lipid nanoparticle (LNP) formulations of the TLR agonists CpG and polyinosinic/polycytidylic (pIpC), with and without Dox, were first prepared, achieving an encapsulation efficiency >75% and a size <140 nm. In vitro studies identified that LNP pIpC was superior to CpG at activating bone marrow-derived immune cell populations (dendritic cells and macrophages) with minimal toxicity. It was also observed that the pIpC formulation can skew macrophage polarization toward the antitumorigenic M1 phenotype and increase macrophage phagocytosis of cancer cells. Upon intratumoral administration, pIpC Dox LNPs led to significant immune cell infiltration and activation. In survival models, the inclusion of Dox into pIpC LNP improved mice survival compared to control. However, addition of Dox did not show significant improvement in mice's survival compared to singly formulated pIpC LNP. This study has illustrated the potential of pIpC LNP formulations in prospective GBM immunotherapeutic regimes. Future studies will focus on optimizing dosage regimen and/or combination with other modalities, including the standard of care (temozolomide), immune checkpoint blockade, or cancer vaccines.
胶质母细胞瘤(GBM)免疫疗法极具挑战性,因为其促肿瘤微环境的特点是免疫细胞水平低且无活性。Toll样受体(TLR)激动剂已成为有效的免疫佐剂,但在作为单一疗法进行临床试验时,未能显示出改善的疗效。我们假设,将TLR激动剂与诱导免疫原性细胞死亡的药物(阿霉素)组合制成纳米颗粒制剂会产生协同作用,从而改善GBM免疫疗法。首先制备了含或不含阿霉素的TLR激动剂CpG和聚肌苷酸/聚胞苷酸(pIpC)的脂质纳米颗粒(LNP)制剂,其包封率>75%,粒径<140 nm。体外研究表明,LNP pIpC在激活骨髓来源的免疫细胞群体(树突状细胞和巨噬细胞)方面优于CpG,且毒性最小。还观察到pIpC制剂可使巨噬细胞极化偏向抗肿瘤的M1表型,并增加巨噬细胞对癌细胞的吞噬作用。瘤内给药后,pIpC阿霉素LNP导致显著的免疫细胞浸润和激活。在生存模型中,与对照组相比,将阿霉素加入pIpC LNP可提高小鼠存活率。然而,与单独配制的pIpC LNP相比,添加阿霉素并未显著提高小鼠存活率。本研究阐明了pIpC LNP制剂在未来GBM免疫治疗方案中的潜力。未来的研究将集中于优化给药方案和/或与其他治疗方式联合,包括标准治疗(替莫唑胺)、免疫检查点阻断或癌症疫苗。