Innate lymphoid cells (ILCs) are crucial in orchestrating immunity and inflammation in the intestine, but their role in other mucosal sites remains poorly understood. This study identifies a population of lung-resident ILCs in mice and humans that express CD90, CD25, CD127, and the IL-33 receptor subunit T1-ST2. These ILCs accumulate in the lungs after influenza virus infection and depletion of these cells results in impaired lung function, airway epithelial integrity, and respiratory tissue remodeling. Administration of amphiregulin, a lung ILC product, restored these defects. The results demonstrate a critical role for lung ILCs in maintaining airway epithelial integrity and tissue homeostasis after influenza virus infection.Innate lymphoid cells (ILCs) are crucial in orchestrating immunity and inflammation in the intestine, but their role in other mucosal sites remains poorly understood. This study identifies a population of lung-resident ILCs in mice and humans that express CD90, CD25, CD127, and the IL-33 receptor subunit T1-ST2. These ILCs accumulate in the lungs after influenza virus infection and depletion of these cells results in impaired lung function, airway epithelial integrity, and respiratory tissue remodeling. Administration of amphiregulin, a lung ILC product, restored these defects. The results demonstrate a critical role for lung ILCs in maintaining airway epithelial integrity and tissue homeostasis after influenza virus infection.