血液系统恶性肿瘤微环境的免疫代谢重塑与治疗耐受
DOI:
https://doi.org/10.62177/fcdt.v2i5.1734关键词:
血液系统恶性肿瘤, 肿瘤微环境, 免疫代谢重塑, 免疫逃逸, 治疗耐受, 细胞治疗摘要
血液系统恶性肿瘤的发生发展并非仅由异常克隆的细胞内在改变驱动。骨髓、淋巴结等组织中的基质细胞、免疫细胞、内皮细胞、细胞外基质、细胞因子及代谢物共同构成动态肿瘤微环境。恶性细胞与微环境双向塑形,通过黏附依赖性保护、旁分泌信号、免疫抑制、缺氧适应和代谢共生维持存活,并经CXCL12/CXCR4、白细胞介素-6/JAK/STAT3、转化生长因子-β等通路及细胞外囊泡和基质重塑形成药物庇护,促进可测量残留病持续和复发。免疫检查点抑制、嵌合抗原受体细胞治疗、CXCR4阻断、髓系细胞重编程及代谢干预已显示应用潜力,但疗效具有病种依赖性,多数联合方案仍处于临床前或早期临床阶段。本文从细胞组分、非细胞网络和时空异质性三个层面评述血液系统恶性肿瘤微环境的免疫代谢重塑及其介导治疗耐受的机制,并分析现有证据边界与转化难点,为分层治疗和时序联合方案设计提供参考。
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录用日期: 2026-09-28
发表日期: 2026-10-04







