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:CAR-T cell therapy in glioblastoma: from αβ to γδ T-cell platforms.
多形性胶质母细胞瘤(GBM)仍是一种高度侵袭性的脑肿瘤,治疗方案有限,生存率低。
多形性胶质母细胞瘤(GBM)仍是一种高度侵袭性的脑肿瘤,治疗方案有限,生存率低。持续的临床失败促使人们关注具有更高特异性和更强细胞毒性的新型免疫策略,其中嵌合抗原受体(CAR)-T细胞疗法已成为领先方法。CAR-T细胞显示出安全性,但由于抗原异质性、免疫抑制性肿瘤微环境(TME)以及向中枢神经系统(CNS)的迁移受限,其疗效有限。CAR-T细胞将不依赖主要组织相容性复合体(MHC)的肿瘤识别与工程化抗原特异性相结合,在选定模型中已证明具有临床前细胞毒性以及与瘤内持久性一致的特征,并具有现货型潜力,使其成为GBM的下一代免疫治疗策略。
Glioblastoma multiforme (GBM) remains a highly aggressive brain tumor with limited treatment options and poor survival. The persistent clinical failure has driven interest in novel, immune-based strategies with higher specificity and greater cytotoxic potency, among which chimeric antigen receptor (CAR)-T-cell therapy has emerged as a leading approach. CAR-T cells demonstrate safety but limited efficacy due to antigen heterogeneity, an immunosuppressive tumor microenvironment (TME), and restricted trafficking to the central nervous system (CNS). CAR-T cells, combining innate major histocompatibility complex (MHC)-independent tumor recognition with engineered antigen specificity, have demonstrated preclinical cytotoxicity and features consistent with intratumoral persistence in selected models, as well as off-the-shelf potential, making them a next-generation immunotherapy strategy for GBM.
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