Identification of STAT3 signaling as a shared pathogenic signature in systemic lupus erythematosus, chronic obstructive pulmonary disease, and asthma.

While patients with systemic lupus erythematosus (SLE) have a higher risk of developing chronic obstructive pulmonary disease (COPD) and asthma, the underlying mechanisms have yet to be elucidated. To this end, by integrating transcriptomic data obtained from blood specimens for each disorder, this study made an effort to investigate shared pathogenic signatures in these three disorders. After identification of shared differentially expressed genes (DEGs), their protein interactions (PPIs) were mapped using a high confidence threshold (0.7). Construction of the networks led to the identification of STAT3 as the central hub gene. Functional enrichment analysis of the shared PPI network of SLE, COPD, and asthma revealed involvement of the shared DEGs in the activation of innate immunity in conjunction with the dysregulation of adaptive immunity, specifically the differentiation of Th1, Th2, and Th17 cells. Moreover, Gene Ontology (GO) analysis highlighted a substantial imbalance between kinase and phosphatase. These observations suggest the STAT3 signaling pathway not only as a pathogenic link between SLE, COPD, and asthma but also as a potential therapeutic target for patients diagnosed with a combination of these disorders.