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在非小细胞肺癌中,IL-17A促进瘤发生,并上调PD-L1的表达

Hua Liao^1,2, Xiaodan Chang^1,3, Lin Gao¹

¹Chronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Journal of translational medicine

|November 18, 2023

概括

干白素-17A (IL-17A) 通过通过ROS/Nrf2/p62通路抑制自,增加PD-L1表达,促进非小细胞肺癌 (NSCLC) 的进展. 向IL-17A可能会影响NSCLC的免疫疗法的有效性.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

瘤微环境对于非小细胞肺癌 (NSCLC) 的发展和免疫治疗反应至关重要.
干白素-17A (IL-17A) 是一种促炎因素,参与瘤免疫反应.

研究的目的:

研究IL-17A在NSCLC进展中的作用和机制.
探索IL-17A,PD-L1和NSCLC中的自之间的关系.

主要方法:

免疫组织化学 (IHC) 检测NSCLC组织中的IL-17A和PD-L1表达.
在体外测试 (伤口愈合,迁移,入侵,殖民地形成,T细胞杀死) 来评估IL-17A功能.
西部斑点,免疫光和IHC研究IL-17A对自和ROS/Nrf2/p62通路的影响.
在体内皮下瘤模型评估IL-17A对瘤生长和免疫治疗的影响.

主要成果:

IL-17A在NSCLC组织中普遍存在,并且与PD-L1表达呈正相关.
IL-17A促进了NSCLC细胞迁移,入侵和殖民地形成,并增强了细胞生存.
IL-17A诱导的ROS,上调Nrf2和p62,抑制了自,并减少了PD-L1降解.
在体内,抗IL-17A抗体减缓了瘤生长;与抗PD-L1结合减少了治疗效果.

结论:

IL-17A通过ROS/Nrf2/p62通路抑制自性,从而促进NSCLC的进展,从而导致PD-L1表达的增加.
调节IL-17A可能会影响NSCLC免疫疗法的疗效.

关键词:

自自是一种自的过程.免疫治疗是一种免疫疗法.互乐金17A是一种中介蛋白.在NSCLCLC中,我们可以看到NSCLCLC.在PD-L1中.

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