← 返回前沿论文

急性髓系白血病中的 T 细胞应答与 T 细胞疗法

英文原题:T-Cell Responses and T-Cell-Based Therapy in Acute Myeloid Leukemia.

查看英文原题

T-Cell Responses and T-Cell-Based Therapy in Acute Myeloid Leukemia.

PubMed 2025/11/17(内容时间) Curr Med Sci Q3 · IF 2(JCR 2025)

研究概要

急性髓系白血病(AML)是一种常见的侵袭性血液癌症,其特征是原始骨髓细胞的异常生长。

中文摘要

急性髓系白血病(AML)是一种常见且侵袭性强的血液癌症,其特征是原始骨髓细胞的异常生长。基因突变阻止了向血液成分的正常分化。潜在病因包括环境因素、辐射和病毒感染。对AML的研究对于增进我们对这种疾病的理解、促进有效治疗方法的开发以及改进早期诊断方法至关重要,最终目标是提高患者的生存率和生活质量。本研究聚焦于AML中的T细胞免疫应答和T细胞免疫治疗。我们收集了CD8+ T细胞、CD4+ T细胞、自然杀伤T(NKT)细胞以及T细胞中的T细胞,并分析了它们在AML中所发挥的作用。AML的长期疾病控制需要多种免疫疗法,包括T细胞受体工程化T细胞(TCR-T)、CAR-T 细胞疗法(CAR-T)和T细胞免疫检查点抑制剂。我们讨论这些治疗方法,并尝试为未来找到更好的AML治疗方案。

展开英文摘要原文

Acute myeloid leukemia (AML) is a common and aggressive blood cancer characterized by the abnormal growth of primitive bone marrow cells. Genetic mutations prevent normal differentiation into blood components. Potential causes include environmental factors, radiation, and viral infections. Research on AML is essential for enhancing our understanding of the disease, facilitating the development of effective treatments, and improving early diagnostic methods to ultimately increase patient survival rates and quality of life. This study focused on the T-cell immune response and T-cell immunotherapy in AML. We collected CD8+ T cells, CD4 + T cells, Natural killer T (NKT) cells, and T cells among the T cells and analyzed the roles that they play in AML. Long-term disease control in AML requires a variety of immunotherapies, including T-cell receptor-engineered T cells (TCR-T), chimeric antigen receptor T-cell therapy (CAR-T), and T-cell immune checkpoint inhibitors. We discuss these treatments and try to find better treatments for AML in the future.

论文信息

作者
Huang ZH、He R
第一作者单位
School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.China
通讯作者单位
School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. ranhe@hust.edu.cn.China
文献类型
综述
期刊
Current medical science2025 Dec
原文标识
PubMed 41247654 · DOI 10.1007/s11596-025-00121-4