We evaluated the role of SLPI in the Alternaria extract-induced expansion of ILC2s and Th2-type airway inflammation via IL-33, using three models: SLPI-deficient mice, an in vivo SLPI knockdown model with shRNA, and an in vitro model utilizing primary human bronchial epithelial cells (HBECs) exposed to Alternaria extract under various conditions, including plasmid transfection. The gene discussed is IL33; the disease is inflammation.