决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Chimeric Antigen Receptor-Macrophages in Pancreatic Cancer: Promise, Pitfalls, and the Path Ahead.
嵌合抗原受体工程化巨噬细胞(CAR-M)正成为免疫治疗中具有变革意义的前沿方向,是胰腺癌的一种有前景的策略。
嵌合抗原受体工程化巨噬细胞(CAR-M)是免疫治疗中新兴的重要方向,也是治疗胰腺癌的一种有前景策略。与用于实体瘤时面临局限的CAR-T 细胞或嵌合抗原受体NK 细胞(CAR-NK)不同,CAR-M兼具先天肿瘤归巢能力和工程化抗原特异性,有望克服这些障碍。近期研究已在胰腺导管腺癌(PDAC)临床前模型中显示令人鼓舞的抗肿瘤活性;然而,关于其持久性、安全性和可扩展性的关键问题仍未解决。尽管存在这些不确定性,CAR-M仍可能推动治疗范式转变:从仅关注直接细胞毒性介导的免疫活化,转向同时整合免疫协调和肿瘤微环境重编程。
Chimeric antigen receptor-engineered macrophages (CAR-Ms) are emerging as a transformative frontier in immunotherapy and represent a promising strategy for pancreatic cancer. Unlike chimeric antigen receptor T-cell (CAR-T) or chimeric antigen receptor natural killer cell (CAR-NK) cells, which encounter limitations when applied to solid tumors, CAR-Ms combine innate tumor-homing capabilities with engineered antigen specificity to overcome these barriers. Recent studies have demonstrated encouraging antitumor activity in preclinical pancreatic ductal adenocarcinoma (PDAC) models; however, key questions remain regarding the persistence, safety, and scalability of these models. Nonetheless, despite these uncertainties, CAR-Ms may represent a paradigm shift from immune activation focused solely on direct cytotoxicity to one that also integrates immune orchestration and tumor microenvironmental reprogramming.
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