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斗细胞淋巴瘤细胞和淋巴瘤相关的巨细胞之间的对话是ibrutinib耐药性的基础

Xiaoqing Sun¹, Caiqin Wang², Jianghua Cao³

¹Department of Intensive Care Medicine (ICU), State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, P.R.China.

Journal of advanced research

|August 21, 2024

概括

淋巴瘤相关的巨细胞 (LAMs) 在地幔细胞淋巴瘤 (MCL) 中驱动易布鲁替尼抗性. 一种CXCR2抑制剂与易布鲁替尼结合,通过向CXCL5/CXCR2轴来逆转耐药性,提供了一个新的治疗策略.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

薄膜细胞淋巴瘤 (MCL) 经常会对伊布鲁替尼治疗产生抗性.
淋巴瘤相关的巨细胞 (LAMs) 与ibrutinib耐药性有关,但尚未得到充分理解.

研究的目的:

调查LAMs在调解MCL中ibrutinib耐药性的作用.
探索潜在的治疗策略,以LAM为目标,以克服抵抗.

主要方法:

在使用多参数流细胞计 (MPFC) 的MCL患者中评估了巨细胞极化 (M1/M2).
开发了一种MCL细胞和LAM细胞的体外共培养模型,以识别抵抗介导细胞因子.
利用RNA测序,西部斑块和异种移植模型来阐明抗性机制,并测试使用CXCR2抑制剂 (SB225002) 的治疗干预措施.

主要成果:

易布鲁替尼抗性MCL患者的M2/M1 LAM比率较高.
共同培养表明M2巨细胞升高,IBRUTINIB IC50增加,以及耐药模型中较高的IL-8/CXCL5水平.
CXCL5/CXCR2轴激活了Akt,p38和STAT3通路,有助于耐药性;联合SB225002和易布鲁替尼治疗增强了亡并抑制了瘤生长.

结论:

M2极化LAM与MCL中的易布鲁替尼抗性有关.
用CXCR2抑制剂准CXCL5/CXCR2轴可以逆转易布鲁替尼抗性.
这表明,克服ibrutinib在MCL中的耐药性是一种有前途的治疗策略.

关键词:

这是一种BTK抑制剂.在CXCL5中,CXCL5是CXCL5的前身.CXCR2CXCR2CXCR2CXCR2CXCR2CXCR2CXCR2C 巨细胞是一个巨细胞.地膜细胞淋巴瘤是什么电阻电阻电阻电阻电阻电阻

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