The lung has an unique epithelial barrier system to protect host from continuous invasion of various harmful particles including viruses and bacteria. Interleukin (IL-)33, an epithelial cytokine, is released from epithelial cells in the lung and drives the type 2 immune response by activating ST2-expressed immune cells in a number of allergic diseases. However, the pathogenic roles of memory-type ST2+CD4+ T cells in such lung inflammation has been unclear. Here we showed that intratracheal administration of IL-33 induced the substantial increase of numbers of tissue-resident memory-type ST2+CD4+ T cells in the lung. Eosinophilic lung inflammation developed sequentially accompanied by enhanced production of IL-5 and IL-13. T cell-deficient Foxn1nu mice and NSG mice exhibited ameliorated eosinophilic inflammation induced by IL-33. Dexamethasone treatment showed small effects on both the cell number and function of memory-type ST2+CD4+ T cells. Taken together, our study provides novel insight into the pathogenesis of eosinophilic lung disease, showing that memory-type ST2+CD4+ T cells are involved in IL-33-induced eosinophilic inflammation and elicited steroid-resistance.