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多巴胺受体1 阻碍ILC2-介导的抗瘤免疫力

Xiangyang Wang¹, Xiangyu Chen², Jierong Chen³

¹Scientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.

Journal of immunology (Baltimore, Md. : 1950)

|September 20, 2023

概括

多巴胺受体1 (DRD1) 抑制了瘤中的2组先天性淋巴细胞 (ILC2) 活动. 缺少DRD1会增强抗瘤免疫力,延缓癌症的进展,而DRD1的激活会加重瘤负担.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
神经科学是一个神经科学.

背景情况:

第二组先天性淋巴细胞 (ILC2s) 在免疫和癌症中具有不同的作用.
在瘤微环境 (TME) 中ILC2s的确切功能是有争议的,并不明确.
控制癌症中的ILC2活性的机制,无论是促进瘤还是抗瘤,都需要阐明.

研究的目的:

研究多巴胺受体1 (DRD1) 在调节TME内的ILC2活性中的作用.
确定DRD1信号对抗瘤免疫和癌症进展的影响.

主要方法:

利用DRD1缺乏的小鼠模型来评估ILC2-介导的免疫反应.
服用选择性DRD1激动剂芬诺多巴姆,以评估其对ILC2s和瘤生长的影响.
在TME中分析了ILC2激活,乙氨基基细胞招募和细胞毒性CD8+T细胞扩张.

主要成果:

DRD1 缺陷导致了 TME 中 ILC2 激活的增强.
丢失DRD1促进了乙氨基的招募和细胞毒性CD8+T细胞扩张.
缺乏DRD1的小鼠显示瘤生长延迟和瘤进展减少.
芬诺多巴姆治疗抑制了ILC2反应,并加剧了瘤负担.

结论:

多巴胺受体1 (DRD1) 在瘤微环境中起到ILC2活动的负调节作用.
DRD1信号抑制了ILC2驱动的抗瘤免疫力.
准DRD1-ILC2轴为癌症免疫治疗提供了一个潜在的策略.

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