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Mammalian Target of Rapamycin Signaling Enhances Ovalbumin-Induced Neutrophilic Airway Inflammation by Promoting Th17 Cell Polarization in Murine Noneosinophilic Asthma Model
Pediatric Allergy, Immunology, and Pulmonology ( IF 0.9 ) Pub Date : 2020-03-17 , DOI: 10.1089/ped.2019.1088
Jinhong Wu 1 , Wenwei Zhong 1 , Hao Zhang 1 , Yong Yin 1
Affiliation  

Background: T helper 17 (Th17) is regarded as key immune cell in the pathogenesis of noneosinophilic asthma (NEA) due to the recruitment of neutrophils into the airways. The mammalian target of rapamycin (mTOR) is an important signaling molecule that plays a critical role in immune regulation. This study focused on mTOR signaling pathway in the regulation of Th17-mediated neutrophilic airway inflammation.

中文翻译:

雷帕霉素信号的哺乳动物靶点通过促进鼠非嗜酸性哮喘模型中的 Th17 细胞极化来增强卵清蛋白诱导的中性粒细胞气道炎症

背景: T 辅助细胞 17 (Th17) 被认为是非嗜酸性粒细胞性哮喘 (NEA) 发病机制中的关键免疫细胞,因为它会将中性粒细胞募集到气道中。哺乳动物雷帕霉素靶蛋白 (mTOR) 是一种重要的信号分子,在免疫调节中起关键作用。本研究侧重于 mTOR 信号通路在调节 Th17 介导的中性粒细胞气道炎症中的作用。
更新日期:2020-03-17
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