免疫疗法诱导的癌症相关纤维细胞的重编程可以促进瘤的进展
Tomoya Yamashita1,2, Haruki Horiguchi1,3, Tsuyoshi Kadomatsu1,4
1Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Genes to cells : devoted to molecular & cellular mechanisms
|October 31, 2024
概括
免疫检查点抑制剂 (ICI) 可以加速癌症的生长. 在黑色素瘤模型中,炎症性癌症相关纤维细胞 (CAFs) 在ICI治疗后与免疫细胞相互作用,促进了这种进展.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
背景情况:
- 免疫检查点抑制剂 (ICI) 是现代癌症免疫治疗的基石.
- 矛盾的是,ICI有时会导致患者的瘤进展加速.
- 这种不良影响背后的机制仍然不完全理解.
研究的目的:
- 研究癌症相关纤维细胞 (CAFs) 在免疫治疗期间瘤进展中的作用.
- 阐明驱动ICI相关癌症加速的细胞和分子机制.
主要方法:
- 使用了一种小鼠突发性黑色素瘤模型.
- 在ICI治疗的背景下对CAF功能进行了机制分析.
- 研究了免疫细胞-CAF交叉通道.
主要成果:
- ICI治疗诱导CAF的炎症性质,促进瘤的进展.
- 来自T细胞的干扰素- (IFN-γ) 刺激了巨细胞产生瘤坏死因子-α (TNF-α).
- 这种细胞因子信号传递促进了CAFs转化为一种前瘤发病性炎症表型.
结论:
- 与癌症相关的纤维细胞在免疫治疗相关的瘤进展中发挥着关键作用.
- CAF和免疫细胞交叉,特别是涉及IFN-γ和TNF-α,是这种现象的关键驱动因素.
- 准CAF-免疫细胞相互作用可能提供减轻ICI诱导癌症加速的策略.
关键词:
癌症免疫疗法免疫疗法更多相关视频
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