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非恶性 T 细胞作为慢性淋巴细胞白血病免疫治疗反应的決定因素:迈向个体化策略

英文原题:Non-Malignant T Cells as Determinants of Immunotherapeutic Response in Chronic Lymphocytic Leukemia: Towards Personalized Strategies.

PubMed 2026/09/14(内容时间) Oncol Res Q2 · IF 4.6(JCR 2025)

研究概要

慢性淋巴细胞白血病(CLL)是一种生物学上异质性的B细胞恶性肿瘤,其中非恶性T淋巴细胞构成肿瘤微环境的关键组成部分,并显著影响疾病演变和治疗反应。

中文摘要

慢性淋巴细胞白血病(CLL)是一种生物学上异质性的B细胞恶性肿瘤,其中非恶性T淋巴细胞构成肿瘤微环境的关键组成部分,并显著影响疾病演变和治疗反应。越来越多的证据表明,CLL相关T细胞不仅参与抗肿瘤反应,还激活促进CLL亚克隆发展的信号。尽管新型靶向治疗,如Bruton酪氨酸激酶(BTK)抑制剂、BTK降解剂、B细胞淋巴瘤2(BCL-2)抑制剂、T细胞衔接器、免疫检查点抑制剂和过继性T细胞疗法具有不同的作用机制,但它们在靶向CLL细胞之外还影响T细胞区室。因此,深入了解T细胞在CLL发生和进展中的作用,对于正确分层免疫治疗策略的获益-风险比至关重要。本综述全面总结了目前关于CLL中T细胞区室改变的知识,并讨论了其临床意义,涉及临床病程和免疫治疗反应。

展开英文摘要原文

Chronic lymphocytic leukemia (CLL) is a biologically heterogeneous B cell malignancy in which non-malignant T lymphocytes constitute a critical component of the tumor microenvironment and significantly influence disease evolution and the therapeutic response. Growing evidence suggests that CLL-associated T cells not only participate in the antitumor response but also activate signals that promote the development of CLL subclones. Although novel targeted therapies, such as Bruton's tyrosine kinase (BTK) inhibitors, BTK degraders, B-cell lymphoma 2 (BCL-2) inhibitors, T cell engagers, immune checkpoint inhibitors, and adoptive T cell therapy have different mechanisms of action, they affect the T cell compartment in addition to targeting CLL cells. Therefore, in-depth knowledge of the role of T cells in the development and progression of CLL is essential for proper stratification of the benefit-to-risk ratio with regard to immunotherapeutic strategies. This review comprehensively summarizes current knowledge on alterations within the T cell compartment in CLL and discusses the clinical implications, regarding clinical course and response to immunotherapy.

论文信息

作者
Kosmaczewska A、Ciszak L
单位
Department of Experimental Therapy, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.Poland
文献类型
综述
期刊
Oncology research2026
原文标识
PubMed 42769825 · DOI 10.32604/or.2026.081365