设计、选择和优化一种能够诱导 T 细胞识别和杀伤癌细胞的抗 TRAIL-R2/抗 CD3 双特异性抗体。
Design, selection and optimization of an anti-TRAIL-R2/anti-CD3 bispecific antibody able to educate T cells to recognize and destroy cancer cells.
机构信息
a Molecular Therapies Unit, Department of Experimental Oncology and Molecular Medicine , Fondazione IRCCS Istituto Nazionale dei Tumori , Milan , Italy.
b Medical Oncology C Unit, Department of Medical Oncology and Hematology , Fondazione IRCCS Istituto Nazionale dei Tumori , Milan , Italy.
出版信息
MAbs. 2018 Oct;10(7):1084-1097. doi: 10.1080/19420862.2018.1494105. Epub 2018 Aug 6.
Recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or TRAIL-receptor agonistic monoclonal antibodies promote apoptosis in most cancer cells, and the differential expression of TRAIL-R2 between tumor and normal tissues allows its exploitation as a tumor-associated antigen. The use of these antibodies as anticancer agents has been extensively studied, but the results of clinical trials were disappointing. The observed lack of anticancer activity could be attributed to intrinsic or acquired resistance of tumor cells to this type of treatment. A possible strategy to circumvent drug resistance would be to strike tumor cells with a second modality based on a different mechanism of action. We therefore set out to generate and optimize a bispecific antibody targeting TRAIL-R2 and CD3. After the construction of different bispecific antibodies in tandem-scFv or single-chain diabody formats to reduce possible immunogenicity, we selected a humanized bispecific antibody with very low aggregates and long-term high stability and functionality. This antibody triggered TRAIL-R2 in an agonistic manner and its anticancer activity proved dramatically potentiated by the redirection of cytotoxic T cells against both sensitive and resistant melanoma cells. The results of our study show that combining the TRAIL-based antitumor strategy with an immunotherapeutic approach in a single molecule could be an effective addition to the anticancer armamentarium.
重组人肿瘤坏死因子相关凋亡诱导配体(TRAIL)或 TRAIL 受体激动性单克隆抗体可促进大多数癌细胞凋亡,而 TRAIL-R2 在肿瘤组织和正常组织之间的差异表达使其可被开发为肿瘤相关抗原。这些抗体作为抗癌药物的应用已经得到了广泛的研究,但临床试验的结果令人失望。观察到的抗癌活性缺乏可能归因于肿瘤细胞对这种治疗类型的内在或获得性耐药。规避耐药性的一种可能策略是用基于不同作用机制的第二种方式攻击肿瘤细胞。因此,我们着手生成和优化靶向 TRAIL-R2 和 CD3 的双特异性抗体。在构建串联-scFv 或单链二价抗体格式的不同双特异性抗体以降低可能的免疫原性之后,我们选择了一种具有非常低聚体和长期高稳定性和功能的人源化双特异性抗体。该抗体以激动剂的方式触发 TRAIL-R2,并且其抗癌活性通过将细胞毒性 T 细胞重新导向对敏感和耐药性黑素瘤细胞的作用而显著增强。我们的研究结果表明,将基于 TRAIL 的抗肿瘤策略与免疫治疗方法结合在单个分子中可能是抗癌武器库的有效补充。
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