Psoriasis is a chronic, immune-mediated inflammatory skin disease driven by complex genetic and cell type-specific mechanisms, with multi-omics studies highlighting contributions from genomics, epigenomics, proteomics, metabolomics, and microbiomics. A recent cell-type-specific analysis identified cebpd as protective in CD8+ S100B+ T cells (OR = 0.795, P = 0.015) and zfp36 as a risk factor in monocytes (OR = 1.214, P = 0.043), underscoring distinct causal effects in immune subsets (PMID:41991682). Diagnostic work also reported a seven-gene model with excellent performance, achieving an AUC of 0.980, supporting biomarker-based stratification. Therapeutically, topical ionic liquid mediated transdermal platform delivery of a CIL-RNP platform and topical GLUT1 gene editing both improved lesion severity and reduced recurrence in mouse models, suggesting a local gene-editing approach may be effective. Overall, psoriasis remains a major disease area for biomarker discovery and mechanism-guided intervention, with recent literature emphasizing integrated multi-omics and targeted skin delivery strategies (PMID:41891974; PMID:41690121).
Genetic susceptibility and biomarkers
- Genome-wide association studies identified susceptibility loci relevant to psoriasis, supporting a strong inherited component in disease risk (PMID:41891974).
- Epigenetic factors regulate psoriasis-related genes and contribute to pathogenesis, linking epigenomics to disease control (PMID:41891974).
- A seven-gene diagnostic model achieved an AUC of 0.980, indicating high accuracy for psoriasis classification and biomarker development (PMID:41991682).
- Higher cebpd expression in CD8+ S100B+ T cells was protective for psoriasis, while higher zfp36 expression in monocytes increased risk (PMID:41991682).
Multi-omics and disease mechanisms
- Multi-omics integration was highlighted as a central strategy for studying psoriasis pathogenesis and biomarker discovery in a 2026 review (PMID:41891974).
- Proteome alterations in skin and plasma were described in psoriasis, pointing to systemic and tissue-level molecular changes (PMID:41891974).
- Metabolome alterations in skin and plasma were also reported, suggesting altered metabolic states accompany inflammation (PMID:41891974).
- Shifts in skin and gut microbial communities were observed in psoriasis, implicating microbiomics in disease-associated immune dysregulation (PMID:41891974).
Therapeutic delivery and gene editing
- Topical administration of the ionic liquid mediated transdermal platform ameliorated psoriasis in a mouse model, supporting noninvasive local delivery (PMID:41690121).
- Topical GLUT1 gene editing improved lesion severity and reduced recurrence risk in mice, indicating a mechanistic role for glucose transport in skin inflammation (PMID:41690121).
- The CIL-RNP platform was used for topical treatment, demonstrating feasibility of transdermal gene-editing delivery for inflammatory skin disease (PMID:41690121).