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放射治疗诱导的免疫反应通过选择性HDAC6抑制增强

Satish Kumar R Noonepalle¹, Scott Grindrod², Nima Aghdam³

¹Department of Oncology, Georgetown University Lombardi Comprehensive Cancer Center, Washington, District of Columbia.

Molecular cancer therapeutics

|August 16, 2023

概括

用一种新型抑制剂向基因组脱乙酶6 (HDAC6) 阻止放射治疗后M2巨细胞的两极分化,增强抗瘤免疫力,减少瘤复发. 这种组合疗法有望改善癌症治疗结果.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
药理学药理学是指药理学的学科.

背景情况:

放射治疗 (RT) 是一种基石癌症治疗,可触发抗瘤免疫力.
RT可以诱导从亲炎性M1巨细胞转变为抗炎性M2巨细胞,促进瘤耐药性和复发.
希斯脱乙酶6 (HDAC6) 参与调节巨细胞两极分化和免疫反应.

研究的目的:

调查使用选择性抑制剂 (SP-2-225) 向HDAC6的潜力,以增强放射治疗的抗瘤作用.
评估HDAC6抑制对放射治疗后瘤微环境内的巨细胞两极分化的影响.

主要方法:

使用了一种新的选择性HDAC6抑制剂SP-2-225,与放射治疗结合使用.
在瘤微环境中评估瘤生长和巨细胞两极分化 (M1/M2比).

主要成果:

使用SP-2-225和放射治疗的联合治疗显著降低了瘤的生长.
治疗提高了瘤内的M1/M2巨细胞比率,表明向抗瘤免疫反应的转变.

结论:

选择性抑制HDAC6可以将巨细胞重新编程为M1表型,从而增强放射治疗诱导的抗瘤免疫反应.
向HDAC6为组合治疗提供了一个可行的策略,以提高放射治疗的疗效和预防瘤复发.

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