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Chronic obstructive pulmonary disease (COPD) is a lung disease caused by limited airflow that leads to difficulty breathing. It is a major chronic disease that affects human quality of life and even endangers life. However, the exact cause of COPD is still unclear. The present study aimed to identify characteristic genes in COPD, assess the level of immune cell infiltration in COPD samples, and explore the association between characteristic genes and infiltrating immune cells. In this paper, we used dataset GSE76925 to identify 452 differentially expressed genes (DEGs) (including 407 downregulated and 45 upregulated DEGs). Gene Ontology (GO) enrichment analysis showed that the functions mainly include leukocyte migration, protein folding, negative regulation of cell activation, transcription regulator complex, collagen−containing extracellular matrix, RNA polymerase II transcription regulator complex, guanyl nucleotide binding, guanyl ribonucleotide binding, ubiquitin protein ligase binding, etc. In the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, pathways identified by DEGs mainly focused on Basal transcription factors, Arachidonic acid metabolism, Nucleocytoplasmic transport, Glutamatergic synapse, Ether lipid metabolism, alpha−Linolenic acid metabolism, etc. Next, we constructed a weighted gene co-expression network, identified six gene modules, found that the module with the highest correlation was the MEturquoise, and obtained 51 hub module genes. Further, 43 overlapping genes were obtained after the intersection of 452 DEGs and 51 hub genes in MEturquoise module, and seven characteristic DEGs (C-DEGs) (LOC649214, LOC440563, LOC643431, LOC642585, KRT18P17, LOC648057 and UBASH3B) were identified by the Least absolute shrinkage and selection operator (LASSO) regression method. In addition, we assessed the infiltration of 28 immune cells in 111 COPD samples and 40 NC samples, calculated and visualized the correlation between the expression of 7 C-DEGs and the infiltration level of 28 immune cells. These results will contribute to our further understanding of the molecular immunopathogenesis of COPD and have potential reference value for the development of molecular drug targets in the future. [ABSTRACT FROM AUTHOR]