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肺气球细胞中ACKR2的选择性表达和意义

Francesca Albano^1,2, Valeria Mollica Poeta^1,2, Lucia Zotti^1,2

¹IRCCS Humanitas Research Hospital, Rozzano, Italy.

Journal for immunotherapy of cancer

|January 22, 2025

概括

准肺气球中的ACKR2可以减少癌症转移. 从肺内皮细胞中删除ACKR2增强了T淋巴细胞的透,阻碍了瘤的扩散.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
细胞生物学细胞生物学

背景情况:

非典型的化学因子受体2 (ACKR2) 通过结合和降解炎症性CC化学因子来调节炎症.
在不同癌症模型中,ACKR2的遗传缺失与瘤生长的增加以及对肺转移的保护有关.
这项研究研究了ACKR2表达及其在肺转移中的作用.

研究的目的:

为了识别肺部表达ACKR2的特定细胞类型.
确定ACKR2在不同内皮细胞中对肺转移的贡献.
探索ACKR2删除对免疫细胞透和转移的影响.

主要方法:

产生可诱导和条件ACKR2淘汰赛小鼠,具有用于体内成像,流细胞计和免疫光的记者基因.
在肺内皮细胞 (ECs) 上进行RNA测序.
使用肺转移 (黑色素瘤,结直肠癌) 和急性肺损伤 (LPS) 的体内模型.
通过FACS分析白细胞透,并通过多重ELISA测量血清化学激素水平.

主要成果:

在大多数器官中,ACKR2通过淋巴内皮细胞 (LEC) 得到表达,但在肺血液内皮细胞 (BEC) 中称为空气细胞.
从EC中选择性删除ACKR2 (ACKR2^ΔCdh5) 保护免受肺转移,而不是从LEC中删除 (ACKR2^ΔProx1).
保护与肺部T淋巴细胞透增加相关;在肺损伤期间,在ACKR2被删除的EC中观察到增强的T淋巴细胞扩散.

结论:

肺空细胞选择性地表达ACKR2,调节白细胞扩散.
在肺血管毛细血管中准ACKR2调节了化学激素的可用性.
通过ACKR2向促进T淋巴细胞扩散,可以减少肺转移.

关键词:

细胞因子细胞因子这是天生的,天生的.瘤微环境 - - 瘤微环境

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