Siriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand; Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Graduate Program in Clinical Pathology, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; Department of Pathology, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Biomed Pharmacother. 2023 Dec;168:115691. doi: 10.1016/j.biopha.2023.115691. Epub 2023 Oct 14.
Chimeric antigen receptor (CAR) T cell therapy targeting B cell maturation antigen (BCMA) has been approved for treating multiple myeloma (MM). Some clinical studies reported suboptimal outcomes, including reduced cytotoxicity of CAR-T cells and tumor evasion through increased expression of programmed death-ligand 1 (PD-L1). To enhance CAR-T cell efficiency and overcome PD-L1-mediated T cell suppression, we developed anti-BCMA-CAR5-T cells equipped with three costimulatory domains and the ability to secrete anti-PD-L1 single-chain variable fragment (scFv) blockade molecules. Anti-BCMA-CAR4-T cells contained a fully human anti-BCMA scFv and three intracellular domains (CD28, 4-1BB, and CD27) joined with CD3ζ. Anti-BCMA-CAR5-T cells were generated by fusing anti-BCMA-CAR4 with anti-PD-L1 scFv. Both anti-BCMA-CAR4-T and anti-BCMA-CAR5-T cells demonstrated comparable antitumor activity against parental MM cells. However, at an effector-to-target ratio of 1:2, only anti-BCMA-CAR5-T cells maintained cytolytic activity against PD-L1 high MM cells, unlike anti-BCMA-CAR4 T cells. Anti-BCMA-CAR5-T cells were specifically activated by BCMA-expressing target cells, resulting in increased CAR-T cell proliferation, release of cytolytic mediators, and pro-inflammatory cytokines. Anti-BCMA-CAR5-T cells demonstrated specific cytotoxicity against BCMA-expressing target cells, leading to decreased target cell numbers, increased CAR-T cell numbers, and preserved CAR expression during antigenic re-stimulation. Interestingly, only anti-BCMA-CAR5-T cells showed reduced PD-1 receptor levels, which correlated with decreased PD-L1 expression on target cells. We successfully generated anti-BCMA-CAR5-T cells capable of secreting anti-PD-L1 scFv. These cells exhibited superior antitumor efficiency, proliferative capacity, and alleviated T-cell exhaustion against MM cells. Further investigation into the antitumor efficacy of anti-BCMA-CAR5-T cells is warranted in ex vivo and clinical research settings.
嵌合抗原受体 (CAR) T 细胞疗法靶向 B 细胞成熟抗原 (BCMA) 已被批准用于治疗多发性骨髓瘤 (MM)。一些临床研究报告了不理想的结果,包括 CAR-T 细胞的细胞毒性降低和通过程序性死亡配体 1 (PD-L1) 的表达增加而导致的肿瘤逃逸。为了提高 CAR-T 细胞的效率并克服 PD-L1 介导的 T 细胞抑制,我们开发了配备三个共刺激结构域和分泌抗 PD-L1 单链可变片段 (scFv) 阻断分子能力的抗 BCMA-CAR5-T 细胞。抗 BCMA-CAR4-T 细胞包含完全人源抗 BCMA scFv 和三个细胞内结构域(CD28、4-1BB 和 CD27)与 CD3ζ 相连。抗 BCMA-CAR5-T 细胞通过融合抗 BCMA-CAR4 与抗 PD-L1 scFv 而产生。抗 BCMA-CAR4-T 和抗 BCMA-CAR5-T 细胞对亲本 MM 细胞均表现出相当的抗肿瘤活性。然而,在效应细胞与靶细胞的比例为 1:2 时,只有抗 BCMA-CAR5-T 细胞能够保持对 PD-L1 高 MM 细胞的细胞毒性,而抗 BCMA-CAR4 T 细胞则不然。抗 BCMA-CAR5-T 细胞仅被表达 BCMA 的靶细胞特异性激活,导致 CAR-T 细胞增殖、细胞毒性介质释放和促炎细胞因子增加。抗 BCMA-CAR5-T 细胞对表达 BCMA 的靶细胞具有特异性细胞毒性,导致靶细胞数量减少、CAR-T 细胞数量增加和抗原再刺激过程中 CAR 表达得到保留。有趣的是,只有抗 BCMA-CAR5-T 细胞显示 PD-1 受体水平降低,这与靶细胞上 PD-L1 表达降低相关。我们成功地产生了能够分泌抗 PD-L1 scFv 的抗 BCMA-CAR5-T 细胞。这些细胞表现出更高的抗肿瘤效率、增殖能力,并减轻了对 MM 细胞的 T 细胞耗竭。在体外和临床研究环境中进一步研究抗 BCMA-CAR5-T 细胞的抗肿瘤疗效是必要的。