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瘤微环境中的CD8+ T细胞调节了乳腺癌内分泌治疗的反应

Fabiana Napolitano¹, Yunguan Wang², Dhivya R Sudhan¹

¹Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, United States of America.

The Journal of clinical investigation

|December 9, 2025

概括

瘤免疫微环境影响激素受体阳性乳腺癌中抗雌激素治疗反应. 与CD8+T细胞相关的CXCL11在雌激素缺乏期间促进癌细胞生长,影响治疗结果.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
内分泌学在内分泌学.

背景情况:

瘤免疫微环境 (TIME) 显著影响癌症治疗的疗效.
TIME在激素受体阳性 (HR+) 乳腺癌对抗雌激素治疗的反应中的作用尚未完全理解.
雌激素剥夺 (ED) 是HR+乳腺癌治疗的关键策略.

研究的目的:

研究TIME在调节HR+乳腺癌中对抗雌激素治疗的反应中的作用.
在缺少雌激素的条件下,探索免疫细胞,化学因子和癌细胞之间的相互作用.

主要方法:

对HR+乳腺癌患者的治疗前和治疗期间活检的分析.
通过H&E染色来评估瘤透淋巴细胞 (TILs).
对于免疫基因表达和细胞概况的RNA测序和循环免疫光学.
空间转录学用于绘制免疫细胞分布和基因签名的地图.
在乳腺癌细胞和CD8+ T细胞的体外共同培养实验.

主要成果:

抗ED的瘤表现出肌层TILs和IFNɣ信号的增加.
抗ED的瘤表现出丰富的CD8+T细胞和增强的免疫基因特征.
化学因子CXCL9,CXCL10,CXCL11和受体CXCR3在耐ED瘤中被上调.
在无雌激素条件下,CXCL11和CD8+T细胞共同培养促进了HR+乳腺癌细胞的生长.
沉默CXCL11受体会减弱对CXCL11和CD8+T细胞的反应中的癌细胞增殖.

结论:

在TIME中CD8+T细胞衍生CXCL11可以在雌激素抑制期间促进HR+乳腺癌细胞的增殖.
这种相互作用表明,TIME 影响抗雌激素疗法耐药性的机制存在.
准CXCL11/CXCR3轴可能代表一种治疗策略,以克服HR+乳腺癌中对雌激素剥夺的抵抗力.

关键词:

乳腺癌乳腺癌是什么?化学因子 (chemokines) 是一种化学物质.药物治疗是药物治疗.免疫学免疫学免疫学在瘤学瘤学.

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