ILC2 cells in the lungs and peritoneal cavity following CLP-induced sepsis showed IL33/suppression of tumorigenicity 2 (ST2), signaling overexpression and expansion of ILC2 in the lungs and provides ILC2-derived IL9, which alleviates sepsis-induced EC pyroptosis through controlling caspase1 activation. This evidence concerns the gene IL33 and Sepsis.