摘要
嵌合抗原受体T细胞(CAR-T)免疫疗法是肿瘤精准靶向治疗的新模式之一。然而,CAR-T输注后出现细胞因子释放综合征(CRS),是限制其治疗效应的关键障碍。巨噬细胞激活、靶肿瘤细胞焦亡可引发白细胞介素-6等炎症因子的释放,而过量的炎症因子可导致内皮细胞过度活化,是CRS升级和发生严重不良事件的关键分子机制。在产生细胞因子的多个环节进行干预以及对嵌合抗原受体分子的结构进行优化是降低CRS的有效策略。
Chimeric antigen receptor T-cell(CAR-T)immunotherapy is one of the new models of tumor targeted therapy.However,the presence of cytokine release syndrome(CRS)after CAR-T infusion is a key obstacle limiting its therapeutic effects.Macrophage activation and pyrosis of target tumor cells can trigger the release of interleukin-6 and other inflammatory factors,and excessive inflammatory factors can lead to excessive activation of endothelial cells,which is a key molecular mechanism for the escalation of CRS and the occurrence of serious adverse events.Intervention in multiple stages of cytokine production and structural optimization of chimeric antigen receptor molecules are effective strategies to reduce CRS.
作者
张丽
向卓
王强
毕经旺
Zhang Li;Xiang Zhuo;Wang Qiang;Bi Jingwang(Graduate School of Jinzhou Medical University,Jinzhou 121001,China;Department of Oncology,Shandong Second Provincial General Hospital,Jinan 250023,China)
出处
《国际肿瘤学杂志》
CAS
2023年第6期377-381,共5页
Journal of International Oncology