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在AML骨髓中乳酸的升高有助于通过GPR81信号传递对巨细胞的极化

Celia A Soto¹, Maggie L Lesch¹, Jennifer L Becker¹

¹University of Rochester School of Medicine, Rochester, New York, United States.

|December 9, 2025

概括

急性髓性白血病 (AML) 的高乳酸水平通过抑制免疫细胞和损害正常血细胞发育,促进癌症的进展. 通过GPR81准乳酸信号传递为AML提供了潜在的新疗法.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
代谢学代谢学代谢学

背景情况:

急性髓性白血病 (AML) 与骨髓微环境 (BMME) 之间的相互作用对于疾病进展和治疗耐药性至关重要.
已知瘤微环境中的代谢物水平变化是导致癌症进展的因素.

研究的目的:

为了研究乳酸的作用,一个关键的代谢物,在白血病骨髓微环境.
探索乳酸对白血病相关巨细胞 (LAMs) 的影响及其作为治疗点的潜力.

主要方法:

对AML患者骨髓血清的代谢分析.
利用一种小鼠AML模型 (爆发性危机慢性髓性白血病 - bcCML) 来研究LAM两极化.
使用缺乏GPR81的小鼠来评估乳酸受体信号传递的作用.

主要成果:

乳酸是AML BMME中最高的代谢物.
通过GPR81传递的乳酸信号驱动LAM两极分化,并直接支持白血病细胞.
乳酸水平升高会损害造血原体的功能,并减少对正常造血的 stromal 支持.

结论:

微环境乳酸是AML诱导的免疫抑制和疾病进展的机制.
GPR81信号代表了AML治疗的新型治疗标.

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