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.
CAR-T（CAR-T）细胞在血液系统恶性肿瘤中的应用推动了这种免疫治疗形式的显著进展。
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
靶向 TRIM29 作为 CAR-NK 细胞效应功能的负调控因子以提升其抗肿瘤疗效：观点
英文原题：Targeting TRIM29 As a Negative Regulator of CAR-NK Cell Effector Function to Improve Antitumor Efficacy of these Cells: A Perspective.
查看英文原题
Targeting TRIM29 As a Negative Regulator of CAR-NK Cell Effector Function to Improve Antitumor Efficacy of these Cells: A Perspective.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
中文摘要
自然杀伤（NK）细胞是固有免疫防御中最重要的细胞之一。与T细胞不同，NK细胞的效应功能不需要预先刺激，也不受MHC限制。因此，嵌合抗原受体（CAR）-NK细胞优于CAR-T 细胞。肿瘤微环境（TME）的复杂性使得有必要探索参与NK细胞负调控的各种途径。通过抑制负调控机制，可以提高CAR-NK细胞的效应功能。在这方面，已知E3泛素连接酶三重基序包含29（TRIM29）参与降低NK细胞细胞毒性和细胞因子产生。此外，靶向TRIM29可能增强CAR-NK细胞的抗肿瘤疗效。本研究讨论了TRIM29对NK细胞活性的负面影响，并提出基因组删除或抑制TRIM29表达作为优化基于CAR-NK细胞免疫治疗的新方法。
展开英文摘要原文
Natural killer (NK) cells are among the most important cells in innate immune defense. In contrast to T cells, the effector function of NK cells does not require prior stimulation and is not MHC restricted.
Therefore, chimeric antigen receptor (CAR)-NK cells are superior to CAR-T cells. The complexity of the tumor microenvironment (TME) makes it necessary to explore various pathways involved in NK cell negative regulation. CAR-NK cell effector function can be improved by inhibiting the negative regulatory mechanisms.
In this respect, the E3 ubiquitin ligase tripartite motif containing 29 (TRIM29) is known to be involved in reducing NK cell cytotoxicity and cytokine production. Also, targeting TRIM29 may enhance the antitumor efficacy of CAR-NK cells. The present study discusses the negative effects of TRIM29 on NK cell activity and proposes genomic deletion or suppression of the expression of TRIM29 as a novel approach to optimize CAR-NK cell-based immunotherapy.
论文信息
- 作者
- Saleh Z、Noroozi M、Vakili ME、Kabelitz D、Nasrollahi H、Kalantar K
- 单位
- Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.Iran
- 文献类型
- 综述 · 非美国政府资助研究
- 期刊
- Current molecular medicine2024
- 原文标识
- PubMed 37218209 · DOI 10.2174/1566524023666230510101525