IL1B is an important driver in COPD, mainly involved in the mechanism where, in the CS-induced pulmonary inflammatory model, IL1B mediated the increasing number of dendritic cells and T-lymphocytes in bronchoalveolar gavage fluid and lung tissue, and these two types of cells could promote the release of IL-6 and IL-17, increasing the recruitment of neutrophils into the airway32,33. This evidence concerns the gene IL6 and chronic obstructive pulmonary disease.