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解开UPR介导的细胞间交叉声:对免疫疗法耐药机制的影响

Si Lu¹, Qimin Zhou², Rongjie Zhao³

¹Department of Head and Neck Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China; Zhejiang Provincial Key Laboratory of Pancreatic Disease, First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China; Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, Hangzhou, China; Institute of Fundamental and Transdisciplinary Research, Zhejiang University, Hangzhou, China.

|March 7, 2025

概括

瘤微环境中的展开蛋白质反应 (UPR) 通过改变瘤和免疫细胞,促进癌症的进展和免疫疗法耐药性. 准UPR通路可能会增强癌症免疫力和治疗疗效.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
在瘤学瘤学.

背景情况:

细胞内膜网膜 (ER) 对于细胞功能,如蛋白质折叠和平衡至关重要.
由错误折叠的蛋白质引起的ER压力激活了展开的蛋白质反应 (UPR).
在瘤微环境 (TME) 中,UPR与瘤进展和免疫逃避有关.

研究的目的:

审查UPR介导的细胞间信号如何影响免疫疗法耐药性.
检查TME内的瘤和免疫细胞中的UPR变化.
突出在癌症免疫治疗中准UPR的治疗潜力.

主要方法:

对ER压力,UPR和癌症免疫力研究的文献综述.
对UPR信号通路 (IRE1α,PERK,ATF6) 的分析.
检查UPR在TME内的瘤细胞和免疫细胞相互作用中的作用.

主要成果:

在TME中的恶性和免疫细胞中观察到持续的UPR激活.
UPR有助于瘤进展,转移和抗瘤免疫力受损.
UPR信号影响免疫治疗的耐药性.

结论:

在调节瘤微环境和免疫反应方面,UPR起着至关重要的作用.
准UPR途径是克服免疫疗法耐药性的有希望的策略.
调节UPR可以提高癌症治疗的疗效.

关键词:

免疫疗法耐药性免疫疗法耐药性瘤微环境是一个微环境.通过UPR进行全日制检查.

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