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利用 NK 细胞开发下一代细胞免疫治疗

英文原题:Harnessing natural killer cells to develop next-generation cellular immunotherapy.

查看英文原题

Harnessing natural killer cells to develop next-generation cellular immunotherapy.

PubMed 2022/08/02(内容时间) Chronic Dis Transl Med

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中文摘要

细胞免疫治疗利用工程化的T细胞、巨噬细胞或自然杀伤(NK)细胞,借助人体自身免疫系统来对抗癌症。与常用于治疗血液系统恶性肿瘤的CAR-T(CAR-T)细胞相比,CAR-NK细胞已展现出显著的治疗效果,同时具有更高的安全性、更低的移植物抗宿主病风险、更少的副作用以及更强的抗肿瘤效力。临床前试验已揭示,过继性CAR-NK细胞疗法在动物模型中具有削减甚至消除血液系统恶性肿瘤和实体瘤的巨大潜力。本文阐述了CAR-NK细胞的设计原理,重点介绍了CAR-NK细胞在临床前测试和临床试验中的最新进展,简要探讨了CAR-NK治疗的主要障碍,并讨论了克服这些挑战的潜在解决方案。鉴于免疫细胞工程基础研究和转化研究的加速进展,CAR-NK细胞疗法有望成为下一代细胞免疫治疗的有力竞争者及重要补充。

展开英文摘要原文

Cellular immunotherapy harnesses the body's own immune system to fight cancer by using engineered T cells, macrophages, or natural killer (NK) cells. Compared to chimeric antigen receptor T (CAR-T) cells that are commonly used to treat hematological malignancies, CAR-NK cells have shown remarkable therapeutic effectiveness while exhibiting enhanced safety, reduced risk of graft-versus-host disease, fewer side effects, and amplified antitumor efficacy.

Preclinical trials have unveiled the high potential of adoptive CAR-NK cell therapy to curtail or even eliminate both hematological malignancies and solid tumors in animal models.

We brought forth herein the design principle of CAR-NK cells, highlighted the latest progress in the preclinical testing and clinical trials of CAR-NK cells, briefly delved into discussed major roadblocks in CAR-NK therapy, and discussed potential solutions to surmount these challenges. Given the accelerated progress in both basic and translational studies on immune cell engineering, CAR-NK cell therapy promises to become a serious contender and important addition to the next-generation cell-based immunotherapy.

论文信息

作者
Liu S、Nguyen K、Park D、Wong N、Wang A、Zhou Y
单位
Center for Translational Cancer Research, Institute of Biosciences and Technology Texas A&M University Houston Texas USA.United States
文献类型
综述
期刊
Chronic diseases and translational medicine2022 Dec
原文标识
PubMed 36420177 · DOI 10.1002/cdt3.40