Besides, in studies of cigarette smoke–induced chronic obstructive pulmonary disease in mice, an increase in all ILC populations was found in bronchoalveolar lavage fluid, especially IL-17 +ILC [21], suggesting that ILC3’s rapid secretion of IL-17 and IL-22 is one of the important mechanisms of pulmonary inflammation. Here, IL17A is linked to chronic obstructive pulmonary disease.