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超高剂量率 (FLASH) 碳离子辐射抑制了Pan02细胞系上的免疫抑制蛋白质表达

Shohei Katsuki¹, Kazumasa Minami¹, Karin Oniwa¹

¹Department of Medical Physics and Engineering, Osaka University Graduate School of Medicine, 1-7 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Journal of radiation research

|December 26, 2024

概括

与传统方法相比,超高剂量速率 (uHDR) 碳离子疗法对癌细胞免疫标记物有明显的影响. 这种新的方法可能会改变DNA损伤修复和内质网膜压力反应,影响癌症治疗策略.

科学领域:

辐射瘤学辐射瘤学
癌症生物学癌症生物学
免疫学免疫学免疫学

背景情况:

超高剂量率 (uHDR) 辐射疗法,或FLASH,显示出保护正常组织的承诺,同时保持抗癌效果.
了解HHDR对癌细胞免疫反应的影响对于优化治疗策略至关重要.

研究的目的:

为了比较免疫相关蛋白质表达 (calreticulin,MHC-I,PD-L1) 在马射线,常规剂量速率 (Conv) 碳离子和 uHDR碳离子照射后的癌细胞上.
调查HHDR碳离子对DNA损伤和内质网膜应激通路的影响.

主要方法:

用玛射线,Conv C-离子 (1.16 Gy/s) 和HDR C-离子 (380 Gy/s) 对B16F10黑色素瘤和Pan02胰腺癌细胞进行辐射.
使用流式细胞计量评估卡尔雷蒂库林 (CRT),MHC-I和PD-L1的表达.
评估内质网膜 (ER) 应激,DNA损伤和修复途径的评估,通过西方抹杀和PCR.

主要成果:

辐射增加了B16F10细胞的CRT和MHC-I;只有C离子增加了Pan02细胞的MHC-I.
在马射线和C离子辐射后,PD-L1表达在B16F10细胞上增加.
值得注意的是,与Conv C-ion相比,HHDR C-ion抑制了Pan02细胞上的PD-L1表达,并证明了与Conv C-ion相比对DNA损伤和ER修复途径的不同影响.

结论:

uHDR碳离子疗法独特地影响癌细胞中的免疫相关蛋白质表达和DNA/ER应激修复途径.
这项研究提供了在HHDR碳离子辐射后免疫相关蛋白质表达变化的第一个证据,为癌症治疗研究开辟了新的途径.

关键词:

一个闪光灯.在PD-L1中.卡莱蒂库林 (CRT) 是一种碳离子束的碳离子束.超高剂量速率的超高剂量速率

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