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:Driving CAR therapies beyond T cells.
嵌合抗原受体(CAR)-T细胞疗法已重塑了血液系统恶性肿瘤的肿瘤免疫治疗,然而在实体瘤中的进展仍然有限。
嵌合抗原受体(CAR)-T 细胞疗法重塑了血液系统恶性肿瘤的癌症免疫治疗格局,但在实体瘤中的进展仍然有限。物理屏障、抗原异质性以及免疫抑制性肿瘤微环境限制了 CAR-T 细胞的活性与持久性,同时安全性问题也使靶点选择变得更加复杂。将 CAR 技术拓展至其他免疫细胞谱系,如巨噬细胞、NK 细胞、TIL(肿瘤浸润淋巴细胞)及非常规 T 细胞,为肿瘤识别、浸润和免疫调节提供了互补机制。本综述重点介绍这些新兴 CAR 平台的最新进展,比较其生物学与转化特征,并阐述将细胞内在特性与 CAR 设计相结合如何指导下一代针对实体瘤的细胞免疫治疗。
Chimeric antigen receptor (CAR)-T cell therapy has reshaped cancer immunotherapy for hematological malignancies, yet progress in solid tumors remains limited. Physical barriers, antigen heterogeneity, and immunosuppressive tumor microenvironment restrict the activity and persistence of CAR-T cells, while safety concerns complicate target selection. Extending CAR technology to alternative immune lineages, such as macrophages, natural killer cells, tumor-infiltrating lymphocytes, and unconventional T cells, offers complementary mechanisms for tumor recognition, infiltration, and immune modulation. This review highlights recent advances in these emerging CAR platforms, compares their biological and translational features, and outlines how integrating cell-intrinsic properties with CAR design may guide the next generation of cellular immunotherapies for solid tumors.
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