上睑下垂
先天性淋巴细胞
炎症
败血症
免疫学
肺
先天免疫系统
医学
生物
炎症体
免疫系统
内科学
作者
Dengming Lai,Jing Tang,Linsong Chen,Erica Fan,Melanie J. Scott,Yuehua Li,Timothy R. Billiar,Mark A. Wilson,Xiangming Fang,Qiang Shu,Jie Fan
标识
DOI:10.1038/s41419-018-0412-5
摘要
Group 2 innate lymphoid cells (ILC2) are one of three subgroups of innate lymphoid cells (ILC1, ILC2, and ILC3), and the major ILC population detected in the lungs. The function of ILC2 in the regulation of lung inflammation remains unclear. In the current study, we explored an important role of ILC2 in protecting lung endothelial cell (EC) from pyroptosis in sepsis-induced acute lung inflammation and the underlying mechanism. Using a cecal ligation and puncture (CLP) mouse sepsis model, we demonstrated that IL-33, which is released in response to sepsis, acting through its receptor ST2 mediates ILC2 expansion in the lungs. We further showed that the increased ILC2 in the lungs secrete IL-9, which in turn prevents lung EC from undergoing pyroptosis, a pro-inflammatory cell death form, by attenuating caspase-1 activation. These findings suggest a previously unidentified innate pathway that negatively regulates lung inflammation following sepsis.
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