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高剂量辐射诱导膀胱癌细胞免疫原性细胞死亡导致树突状细胞激活。

High-dose radiation-induced immunogenic cell death of bladder cancer cells leads to dendritic cell activation.

机构信息

School of Biology and Engineering/School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.

Engineering Center of Cellular Immunotherapy of Guizhou Province, Guiyang, China.

出版信息

PLoS One. 2024 Sep 4;19(9):e0307024. doi: 10.1371/journal.pone.0307024. eCollection 2024.

DOI:10.1371/journal.pone.0307024
PMID:39231199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11373825/
Abstract

Radiotherapy is a commonly used method in the treatment of bladder cancers (BC). Radiation-induced immunogenic cell death (ICD) is related to the immune response against cancers and their prognoses. Even though dendritic cells (DC) act as powerful antigen-presenting cells in the body, their precise role in this ICD process remains unclear. Accordingly, an in vitro study was undertaken to ascertain whether high-dose radiation-induced ICD of BC cells could regulate the immune response of DC. The results indicated that high-dose radiation treatments of BC cells significantly increased their levels of apoptosis, blocked their cell cycle in the G2/M phase, increased their expression of ICD-related proteins, and upregulated their secretion of CCL5 and CCL21 which control the directed migration of DC. It was also noted that expression of CD80, CD86, CCR5, and CCR7 on DC was upregulated in the medium containing the irradiated cells. In conclusion, the present findings illustrate that high-dose radiation can induce the occurrence of ICD within BC cells, concomitantly resulting in the activation of DC. Such findings could be of great significance in increasing the understanding how radiotherapy of BC may work to bring about reductions in cell activity and how these processes in turn lead to immunoregulation of the function of DC.

摘要

放射疗法是治疗膀胱癌(BC)的常用方法。辐射诱导的免疫原性细胞死亡(ICD)与针对癌症及其预后的免疫反应有关。尽管树突状细胞(DC)在体内充当强大的抗原呈递细胞,但它们在该 ICD 过程中的确切作用仍不清楚。因此,进行了一项体外研究,以确定高剂量辐射诱导的 BC 细胞 ICD 是否可以调节 DC 的免疫反应。结果表明,BC 细胞的高剂量辐射处理显着增加了细胞凋亡水平,阻止了细胞在 G2 / M 期的细胞周期,增加了 ICD 相关蛋白的表达,并上调了它们分泌的 CCL5 和 CCL21,从而控制 DC 的定向迁移。还注意到,含有照射细胞的培养基中 DC 上的 CD80、CD86、CCR5 和 CCR7 的表达上调。总之,这些发现表明高剂量辐射可以诱导 BC 细胞中 ICD 的发生,同时激活 DC。这些发现对于增加对 BC 放射疗法如何降低细胞活性以及这些过程如何反过来导致 DC 功能的免疫调节的理解具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/f8c51cba0a67/pone.0307024.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/1f22d497c848/pone.0307024.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/b1d88d5139f0/pone.0307024.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/a3f2461fcb69/pone.0307024.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/f20b2dba0a51/pone.0307024.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/179d89f5a9f0/pone.0307024.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/f8c51cba0a67/pone.0307024.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/1f22d497c848/pone.0307024.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/b1d88d5139f0/pone.0307024.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/a3f2461fcb69/pone.0307024.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/f20b2dba0a51/pone.0307024.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/179d89f5a9f0/pone.0307024.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f0d/11373825/f8c51cba0a67/pone.0307024.g006.jpg

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