下调和上调
先天性淋巴细胞
白细胞介素33
刺激
神经肽1
免疫学
免疫系统
细胞因子
生物
白细胞介素
先天免疫系统
内分泌学
癌症研究
生物化学
基因
血管内皮生长因子受体
血管内皮生长因子
作者
Ying Wang,Gaoyu Liu,Qianqian Wang,Pan Zhou,Lijuan Zhang,Qiang Li,Jie Zhou
摘要
Abstract Group 2 innate lymphoid cells (ILC2s) play critical roles in driving the pathogenesis of allergic airway inflammation. The mechanisms underlying the regulation of ILC2s remain to be fully understood. Here, we identified neuropilin‐1 (NRP1) as a surface marker of ILC2s in response to IL‐33 stimulation. NRP1 was abundantly expressed in ILC2s from lung under steady state, which was significantly reduced upon IL‐33 stimulation. ILC2s with high expression of NRP1 (NRP1 high ) displayed lower response to IL‐33, as compared with NRP1 low ILC2s. Transcriptional profiling and flow cytometric analysis showed that downregulation of AKT–mTOR signalling participated in the diminished functionality of NRP1 high ILC2s. These observations revealed a potential role of NRP1 in ILC2s responses under allergic inflammatory condition.
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