This review proposes a core immunological proposition: PCD serves as a key "bridge," amplifying the innate immune response through mechanisms such as DAMPs release, NLRP3 inflammasome, and immunogenic cell death on one hand, while driving adaptive immune disorders in COPD by affecting antigen presentation, Th1/Th2/Th17 imbalance, T cell exhaustion, and "autoimmune-like" responses on the other hand. This evidence concerns the gene NLRP3 and chronic obstructive pulmonary disease.