Lu Yu-Jen, Vayalakkara Reesha Kakkadavath, Dash Banendu Sunder, Hu Shang-Hsiu, Premji Thejas Pandaraparambil, Wu Chun-Yuan, Shen Yang-Jin, Chen Jyh-Ping
Department of Neurosurgery, Chang Gung Memorial Hospital at Linkou, Kwei-San, Taoyuan 33305, Taiwan.
College of Medicine, Chang Gung University, Kwei-San, Taoyuan 33302, Taiwan.
Pharmaceutics. 2024 Aug 13;16(8):1064. doi: 10.3390/pharmaceutics16081064.
Glioblastoma multiforme (GBM) is the most severe form of brain cancer and presents unique challenges to developing novel treatments due to its immunosuppressive milieu where receptors like programmed death ligand 1 (PD-L1) are frequently elevated to prevent an effective anti-tumor immune response. To potentially shift the GBM environment from being immunosuppressive to immune-enhancing, we engineered a novel nanovehicle from reduced graphene oxide quantum dot (rGOQD), which are loaded with the immunomodulatory drug resiquimod (R848) and conjugated with an anti-PD-L1 antibody (aPD-L1). The immunomodulatory rGOQD/R8/aPDL1 nanoparticles can actively target the PD-L1 on the surface of ALTS1C1 murine glioblastoma cells and release R848 to enhance the T-cell-driven anti-tumor response. From in vitro experiments, the PD-L1-mediated intracellular uptake and the rGOQD-induced photothermal response after irradiation with near-infrared laser light led to the death of cancer cells and the release of damage-associated molecular patterns (DAMPs). The combinational effect of R848 and released DAMPs synergistically produces antigens to activate dendritic cells, which can prime T lymphocytes to infiltrate the tumor in vivo. As a result, T cells effectively target and attack the PD-L1-suppressed glioma cells and foster a robust photothermal therapy elicited anti-tumor immune response from a syngeneic mouse model of GBM with subcutaneously implanted ALTS1C1 cells.
多形性胶质母细胞瘤(GBM)是最严重的脑癌形式,由于其免疫抑制环境,如程序性死亡配体1(PD-L1)等受体经常升高以阻止有效的抗肿瘤免疫反应,这给开发新疗法带来了独特挑战。为了可能将GBM环境从免疫抑制转变为免疫增强,我们用还原氧化石墨烯量子点(rGOQD)设计了一种新型纳米载体,其负载免疫调节药物瑞喹莫德(R848)并与抗PD-L1抗体(aPD-L1)偶联。免疫调节性rGOQD/R8/aPDL1纳米颗粒可以主动靶向ALTS1C1小鼠胶质母细胞瘤细胞表面的PD-L1并释放R848以增强T细胞驱动的抗肿瘤反应。体外实验表明,PD-L1介导的细胞内摄取以及近红外激光照射后rGOQD诱导的光热反应导致癌细胞死亡并释放损伤相关分子模式(DAMP)。R848和释放的DAMP的联合作用协同产生抗原以激活树突状细胞,树突状细胞可启动T淋巴细胞在体内浸润肿瘤。结果,T细胞有效地靶向并攻击PD-L1抑制的胶质瘤细胞,并在皮下植入ALTS1C1细胞的GBM同基因小鼠模型中促进强大的光热疗法引发的抗肿瘤免疫反应。