Neuroimmune-related differentially expressed genes in psoriasis: A bioinformatics analysis reveals potential biomarkers for diagnosis and treatment

Background Psoriasis is a chronic inflammatory skin disease in which neuroimmune interactions are increasingly recognized but remain insufficiently defined. Objective To elucidate neuroimmune mechanisms implicated in psoriasis pathogenesis and identify candidate biomarkers and therapeutic targets. Methods Publicly available psoriasis transcriptomic datasets from the Gene Expression Omnibus (GEO) were analyzed. Neuroimmune-related differentially expressed genes (NRDEGs) were screened, followed by functional enrichment analyses. Supervised diagnostic models (logistic regression, support vector machine, least absolute shrinkage and selection operator [LASSO], and random forest) were constructed. Immune cell infiltration was estimated and correlated with NRDEG expression. Protein–protein interaction networks were built, and key genes were queried against drug/active-ingredient resources. Results Sixty-eight NRDEGs were identified in psoriatic tissue. These genes were significantly enriched in immune and inflammatory pathways, including NF-κB and IL-17 signaling. Diagnostic models based on NRDEGs achieved high predictive performance across algorithms. Five key genes—ENO2, SELL, GREM2, IL1B, and LCN2—were differentially expressed between patients and controls and showed strong associations with inferred immune cell infiltration in lesions. Network analyses prioritized hub genes and mapped them to potential drug active ingredients, suggesting avenues for pharmacologic modulation of neuroimmune pathways. Conclusions Integrated bioinformatics highlights a prominent neuroimmune signature in psoriasis, nominating NRDEGs—particularly ENO2, SELL, GREM2, IL1B, and LCN2—as candidate biomarkers for diagnosis and potential therapeutic intervention. Further experimental and clinical studies are warranted to define causal roles, clarify dynamics during disease progression, and evaluate responses to targeted therapies.