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多omics概况显示微环境改造是家尘诱导的肺癌进展的关键驱动因素

Shams Al-Azzam^1,2, Isabella Stuewe^2,3, Sunandini Sharma^4,5

¹Biomedical Sciences Graduate Program, University of California San Diego, La Jolla, CA, USA.

bioRxiv : the preprint server for biology

|October 3, 2025

概括

长期暴露于室内灰尘虫会通过抑制免疫反应加速肺癌的发展. 鉴定出interleukin-17A (IL-17A) 是这一过程中的关键调解者,突出显示了过敏和癌症进展之间的联系.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
肺部病理学肺部病理学

背景情况:

长期暴露于家用灰尘虫 (HDM) 会导致肺炎和DNA损伤.
对于HDM对肺癌发展的影响还不太清楚.

研究的目的:

调查慢性HDM暴露对肺癌进展的影响.
阐明HDM驱动的瘤促进背后的分子机制.

主要方法:

使用了全基因组测序,RNA测序和DNA甲基化分析.
在肺上皮细胞系和小鼠 орто型肺癌模型中评估了HDM的影响.
在正常的肺组织和瘤中分析了基因表达和表观遗传变化.

主要成果:

在不增加突变负担的情况下,HDM加速了瘤生长.
在正常的肺部中,HDM诱导了前炎和免疫激活,但在瘤中抑制了T细胞反应和抗原呈现.
免疫解密揭示了髓质丰富和淋巴细胞抑制,减少了细胞毒性T和NK细胞的特征.
HDM的瘤促进依赖于介乐金-17A (IL-17A),但不是介乐金-1b (IL-1b).

结论:

长期暴露于空气过敏原会重塑肺部的微环境.
HDM促进免疫抑制并加速肺癌的进展.
IL-17A是HDM驱动的肺瘤促进的关键调解者.

关键词:

室内灰尘虫是什么意思慢性炎症是一种慢性炎症.肺癌是一种肺癌.肺部免疫微环境是一个微环境.鼠标模型鼠标模型鼠标模型多个主题的个人资料.

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