CAR-T（CAR-T）细胞疗法在非肿瘤性疾病中的应用
Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
癌症-免疫循环的合成调控：CAR-T 细胞治疗
英文原题：Synthetic manipulation of the cancer-immunity cycle: CAR-T cell therapy.
查看英文原题
Synthetic manipulation of the cancer-immunity cycle: CAR-T cell therapy.
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中文摘要
针对癌症的合成免疫始于将嵌合抗原受体（CAR）工程化应用于自体T细胞。CAR-T 细胞疗法易于进行分子工程改造，可绕过癌症免疫循环中的障碍，例如内源性抗原呈递、免疫启动及天然免疫检查点对免疫应答的限制。本文综述CAR-T 设计，以及驱动CAR-T 效应活性持续并发挥抗肿瘤功能的机制，并讨论针对血液系统恶性肿瘤和实体瘤、旨在通过多种机制干预提升抗肿瘤功能的工程化策略。通过改造细胞迁移、抗原识别、共刺激，并加入合成基因或基因线路，开展基因敲除及碱基编辑，从而精细调控复杂功能，这种多样化工程改造能力可以说是操控患者癌症免疫循环最强大的手段。
展开英文摘要原文
Synthetic immunity to cancer has been pioneered by the application of chimeric antigen receptor (CAR) engineering into autologous T cells. CAR T cell therapy is highly amenable to molecular engineering to bypass barriers of the cancer immunity cycle, such as endogenous antigen presentation, immune priming, and natural checkpoints that constrain immune responses.
Here, we review CAR T cell design and the mechanisms that drive sustained CAR T cell effector activity and anti-tumor function.
We discuss engineering approaches aimed at improving anti-tumor function through a variety of mechanistic interventions for both hematologic and solid tumors. The ability to engineer T cells in such a variety of ways, including by modifying their trafficking, antigen recognition, costimulation, and addition of synthetic genes, circuits, knockouts and base edits to finely tune complex functions, is arguably the most powerful way to manipulate the cancer immunity cycle in patients.
论文信息
- 作者
- Singh N、Maus MV
- 第一作者单位
- Division of Oncology, Washington University in St Louis School of Medicine, St. Louis, MO 63110, USA. Electronic address: nathan.singh@wustl.edu.United States
- 通讯作者单位
- Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA 02114, USA. Electronic address: mvmaus@mgh.harvard.edu.United States
- 文献类型
- 综述
- 期刊
- Immunity2023 Oct 10
- 原文标识
- PubMed 37820585 · DOI 10.1016/j.immuni.2023.09.010