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在口腔状细胞癌中,慢性ISG15暴露加速CD8+T细胞功能障碍,同时增加PD-1阻断敏感性

Yu-Lin Chen¹, Amir Yousif², Chung-Hsing Chen³

¹National Health Research Institutes, Miaoli County, Taiwan.

Cancer immunology research

|August 29, 2025

概括

干扰素刺激的15基因 (ISG15) 在头部和部癌症中促进T细胞耗尽. 然而,这些耗尽的T细胞仍然对PD-1阻断免疫疗法有反应,这表明ISG15是预测生物标志物.

科学领域:

免疫学
癌症学
分子生物学

背景情况:

免疫疗法对头部和部状细胞癌 (HNSCC) 是有前途的,但观察到的反应有限.
在口腔状细胞癌 (OSCC) 中,干扰素刺激的15 (ISG15) 基因表达升高可能会阻碍治疗疗效.
作为免疫疗法耐药性的关键因素,分泌的ISG15在T细胞衰竭中的作用尚不完全理解.

研究的目的:

研究分泌的ISG15在CD8+T细胞功能障碍中的特定作用及其对HNSCC免疫疗法的影响.
确定ISG15受损的T细胞是否保持对PD-1阻塞治疗的反应.
评估ISG15作为预测HNSCC免疫治疗反应的潜在生物标志物.

主要方法:

对人类OSCC数据集进行ISG15丰富分析.
开发一种新的体外T细胞功能障碍模型.
使用免疫能力强的OSCC小鼠模型.
评估ISG15暴露对CD8+T细胞功能和瘤生长的影响.
评估PD-1阻断在ISG15表达瘤中的有效性.

主要成果:

与非瘤组织相比,ISG15在OSCC瘤中显著增加.
长时间的ISG15暴露通过依赖细胞内核的机制诱导了CD8+ T细胞功能障碍.
表达ISG15的OSCC瘤呈现出加速生长和功能受损的CD8+ T细胞.
在ISG15的存在下,PD-1阻塞显著减缓了瘤的进展,并恢复了T细胞功能.

结论:

慢性ISG15暴露会促进HNSCC中的CD8+T细胞功能障碍.
受到ISG15损害的T细胞对PD-1阻断疗法保持反应.
ISG15是识别可能受益于PD-1阻塞的HNSCC患者的潜在生物标志物.

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