Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis article

Dengming Lai, Jing Tang, Linsong Chen, Erica K. Fan, Melanie J. Scott, Yuehua Li, Timothy R. Billiar, Mark A. Wilson, Xiangming Fang*, Qiang Shu, Jie Fan

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


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.

Original languageEnglish
Article number369
JournalCell Death and Disease
Issue number3
StatePublished - 1 Mar 2018
Externally publishedYes


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