【Objectives】To develop a group 2 innate lymphoid cell（ILC2）- dominant allergic airway inflammation model in wild type C57BL/6 and T/B cell- deficient Rag1-/- mice. 【Methods】 Female C57BL/6 and Rag1-/- mice were randomly divided into control and model groups. The mice in model groups were administered intratracheally with 1 μg IL-33 in 20 μL H2O on days 1，3 and 5，and the control mice were administered accordingly with 20 μL H2O. On day 6，the mice were sacrificed for collection of bronchoalveolar lavage fluid（BALF）and the lungs. The pulmonary inflammation in mice was evaluated by pathological staining for lung tissues，ELISA for levels of cytokines in BALF，and flow cytometry analyses of ILC2 and inflammatory cells. 【Results】 Both the C57BL/6 and Rag1-/- mice with the treatment of IL- 33 exhibited obvious eosinophilic airway inflammation in peri-tracheal area（P < 0.05）and goblet cell hyperplasia in airway epithelium（P < 0.05）. Compared with the control mice，numbers of eosinophils（P < 0.05）and neutrophils（P < 0.05） as well as levels of IL-5（P < 0.05）and IL-13（P < 0.05）in BALF were increased in the model group. In addition ， significantly higher levels of ILC2 were found in lung tissues of the model mice. 【Conclusion】 The ILC2-dominant allergic airway inflammation was successfully developed in both C57BL/6 and Rag1-/- mice，which provided the approach to investigate the role of ILC2 in asthma and allergic rhinitis.