Innate lymphoid cells (ILCs) are critical for maintaining tissue homeostasis in the lungs after infection with influenza virus. This study identifies a population of lung-resident ILCs in both mice and humans that express CD90, CD25, CD127, and T1-ST2. These ILCs accumulate in the lungs after influenza infection and are essential for restoring airway epithelial integrity and tissue homeostasis. Depletion of these ILCs leads to impaired lung function, loss of airway epithelial integrity, and defective airway remodeling. Administration of amphiregulin, a product of these ILCs, restores lung function and promotes tissue remodeling. ILCs are a diverse group of immune cells that play a role in regulating immunity and inflammation in the gut and other mucosal tissues. In the lungs, ILCs resemble nuocytes and natural helper cells (NHCs) in their surface markers and cytokine production. These ILCs express IL-5 and IL-13 in response to IL-33 and are critical for maintaining airway epithelial barrier function. The development of lung ILCs requires the transcription factor Id2 but is independent of microbial signals. In humans, similar ILC populations are found in the respiratory tract and lung parenchyma. These ILCs express CD25, CD127, and IL-33R, indicating they are nuocyte- or NHC-like ILCs. The study shows that ILCs in the lungs are essential for maintaining tissue homeostasis after influenza infection. Depletion of ILCs results in impaired lung function, loss of airway epithelial integrity, and defective airway remodeling. However, administration of amphiregulin restores lung function and promotes tissue repair. The study also shows that ILCs produce amphiregulin, which is critical for restoring airway epithelial integrity and lung function after influenza infection. Amphiregulin is a member of the epidermal growth factor family and plays a role in tissue repair and remodeling. The findings suggest that ILCs are essential for maintaining lung homeostasis after infection with influenza virus. The study highlights the importance of ILCs in regulating immune responses and tissue homeostasis in the lungs.Innate lymphoid cells (ILCs) are critical for maintaining tissue homeostasis in the lungs after infection with influenza virus. This study identifies a population of lung-resident ILCs in both mice and humans that express CD90, CD25, CD127, and T1-ST2. These ILCs accumulate in the lungs after influenza infection and are essential for restoring airway epithelial integrity and tissue homeostasis. Depletion of these ILCs leads to impaired lung function, loss of airway epithelial integrity, and defective airway remodeling. Administration of amphiregulin, a product of these ILCs, restores lung function and promotes tissue remodeling. ILCs are a diverse group of immune cells that play a role in regulating immunity and inflammation in the gut and other mucosal tissues. In the lungs, ILCs resemble nuocytes and natural helper cells (NHCs) in their surface markers and cytokine production. These ILCs express IL-5 and IL-13 in response to IL-33 and are critical for maintaining airway epithelial barrier function. The development of lung ILCs requires the transcription factor Id2 but is independent of microbial signals. In humans, similar ILC populations are found in the respiratory tract and lung parenchyma. These ILCs express CD25, CD127, and IL-33R, indicating they are nuocyte- or NHC-like ILCs. The study shows that ILCs in the lungs are essential for maintaining tissue homeostasis after influenza infection. Depletion of ILCs results in impaired lung function, loss of airway epithelial integrity, and defective airway remodeling. However, administration of amphiregulin restores lung function and promotes tissue repair. The study also shows that ILCs produce amphiregulin, which is critical for restoring airway epithelial integrity and lung function after influenza infection. Amphiregulin is a member of the epidermal growth factor family and plays a role in tissue repair and remodeling. The findings suggest that ILCs are essential for maintaining lung homeostasis after infection with influenza virus. The study highlights the importance of ILCs in regulating immune responses and tissue homeostasis in the lungs.