Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 USA.
Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Sci Signal. 2024 Jul 23;17(846):eadp8569. doi: 10.1126/scisignal.adp8569.
Chimeric antigen receptor (CAR) T cells have been used to successfully treat various blood cancers, but adverse effects have limited their potential. Here, we developed chimeric adaptor proteins (CAPs) and CAR tyrosine kinases (CAR-TKs) in which the intracellular ζ T cell receptor (TCRζ) chain was replaced with intracellular protein domains to stimulate signaling downstream of the TCRζ chain. CAPs contain adaptor domains and the kinase domain of ZAP70, whereas CAR-TKs contain only ZAP70 domains. We hypothesized that CAPs and CAR-TKs would be more potent than CARs because they would bypass both the steps that define the signaling threshold of TCRζ and the inhibitory regulation of upstream molecules. CAPs were too potent and exhibited high tonic signaling in vitro. In contrast, CAR-TKs exhibited high antitumor efficacy and significantly enhanced long-term tumor clearance in leukemia-bearing NSG mice as compared with the conventional CD19-28ζ-CAR-T cells. CAR-TKs were activated in a manner independent of the kinase Lck and displayed slower phosphorylation kinetics and prolonged signaling compared with the 28ζ-CAR. Lck inhibition attenuated CAR-TK cell exhaustion and improved long-term function. The distinct signaling properties of CAR-TKs may therefore be harnessed to improve the in vivo efficacy of T cells engineered to express an antitumor chimeric receptor.
嵌合抗原受体 (CAR) T 细胞已被成功用于治疗各种血液癌症,但不良反应限制了其应用潜力。在这里,我们开发了嵌合衔接蛋白 (CAP) 和 CAR 酪氨酸激酶 (CAR-TK),其中细胞内 ζ 链 T 细胞受体 (TCRζ) 被细胞内蛋白结构域取代,以刺激 TCRζ 下游的信号转导。CAP 包含衔接结构域和 ZAP70 的激酶结构域,而 CAR-TK 仅包含 ZAP70 结构域。我们假设 CAP 和 CAR-TK 会比 CAR 更有效,因为它们可以绕过定义 TCRζ 信号阈值的步骤和上游分子的抑制调节。CAP 过于有效,在体外表现出高持续信号。相比之下,CAR-TK 与传统的 CD19-28ζ-CAR-T 细胞相比,在白血病荷瘤 NSG 小鼠中表现出更高的抗肿瘤疗效和显著增强的长期肿瘤清除率。CAR-TK 的激活方式不依赖于激酶 Lck,与 28ζ-CAR 相比,其磷酸化动力学较慢,信号持续时间较长。Lck 抑制减弱了 CAR-TK 细胞衰竭,改善了长期功能。因此,CAR-TK 的独特信号特性可被利用来提高表达抗肿瘤嵌合受体的 T 细胞在体内的疗效。