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AML/MDS 细胞治疗的最新进展:探索固有免疫细胞在 AML/MDS 中的治疗潜力

英文原题:Recent advances of cell therapies for AML/MDS: exploring the therapeutic potential of innate immune cells in AML/MDS.

查看英文原题

Recent advances of cell therapies for AML/MDS: exploring the therapeutic potential of innate immune cells in AML/MDS.

PubMed 2025/11/21(内容时间) Int J Hematol Q3 · IF 1.9(JCR 2025)

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中文摘要

免疫疗法已经彻底改变了癌症治疗,但检查点抑制剂和 CAR-T 细胞在急性髓系白血病(AML)和骨髓增生异常综合征(MDS)中显示出有限的疗效。这种有限的疗效主要是由于缺乏谱系特异性抗原以及存在抑制性微环境。固有免疫提供了一种有前景的替代方案,因为它不依赖于新抗原发挥作用。巨噬细胞、树突状细胞和自然杀伤(NK)细胞等关键参与者不仅能消除恶性细胞,还能重塑微环境以增强抗白血病活性。本综述重点介绍了在理解 AML 和 MDS 中固有免疫机制方面的最新进展,并探讨了旨在利用这些通路的治疗策略,以期拓宽免疫疗法的范围。

展开英文摘要原文

Immunotherapy has revolutionized cancer treatments, yet checkpoint inhibitors and CAR-T cells have shown limited efficacy in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). This limited efficacy is primarily due to the absence of lineage-specific antigens and the presence of suppressive microenvironments. Innate immunity offers a promising alternative, as it acts independently of neoantigens.

The key players such as macrophages, dendritic cells, and natural killer (NK) cells not only eliminate malignant cells but also remodel the microenvironment to enhance antileukemic activity. This review highlights recent advances in understanding innate immune mechanisms in AML and MDS and explores therapeutic strategies designed to leverage these pathways, aiming to broaden the scope of immunotherapy.

论文信息

作者
Chang YH、Goyama S
第一作者单位
Division of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.Japan
通讯作者单位
Division of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan. goyama@edu.k.u-tokyo.ac.jp.Japan
文献类型
综述
期刊
International journal of hematology2025 Nov 21
原文标识
PubMed 41269494 · DOI 10.1007/s12185-025-04113-x