Chronic obstructive pulmonary disease (COPD) is characterized by restricted airflow that leads to significant respiratory difficulties. This progressive disease often results in diminished pulmonary function and the onset of additional respiratory conditions. Autophagy, a critical cellular homeostasis mechanism, plays a significant role in the exacerbation of COPD. In this study, we utilized various bioinformatics tools to identify autophagy-related genes activated by smoking in individuals with COPD. Furthermore, we explored the immune landscape of COPD through these genes, analyzing cell communication patterns using scRNA-seq data. This analysis focused on key pathways between epithelial cells and other cellular subpopulations with different autophagy scores, essential for understanding the initiation and progression of COPD.