Psoriasis
ICD-11: EA90
Disease Overview
Psoriasis is a chronic immune-mediated skin disease characterized by hyperproliferation of keratinocytes, epidermal thickening, and inflammatory infiltrate. IL-23/Th17 axis is central; TNF and NF-κB pathways are therapeutic targets. Heritability ~60–70%; SNP-based h² ~0.28. Key genes include HLA-C*06:02, IL23R, and genes in the IL-23/Th17 pathway. Trauma, infection, stress, and medications can trigger flares. Comorbidities include psoriatic arthritis, cardiovascular disease, and metabolic syndrome.
Onset can occur in adolescence; psychosocial impact is substantial. UV and topical treatments are first-line.
Genetic Architecture Summary
| Gene | Variant | GWAS p | Evidence | Strength |
|---|---|---|---|---|
| HLA-C | rs10484554 | 1.0e-100 | HLA-C*06:02 strongest risk allele; antigen presentation | 0.95 |
| IL23R | rs11209026 | 1.0e-30 | IL-23 receptor; Th17 differentiation | 0.9 |
Heritability
h² SNP: 0.28 — Psoriasis GWAS meta-analyses (2020)
PRS notes: PRS correlates with severity; transferability across ancestries limited.
Exposure Modifier Panel
| Exposure | Direction | Strength | Confidence | Mechanism hypothesis |
|---|---|---|---|---|
| psychosocial-stress | amplify | 0.75 | HIGH | — |
| uv-radiation | buffer | 0.7 | HIGH | Phototherapy improves lesions |
Population Equity Notes
GWAS ancestry breakdown: European-dominated discovery.
Transferability notes: HLA-C*06:02 replicated across ancestries; non-HLA loci vary.
Data gaps: Multi-ancestry GWAS and G×E.
Tissue Context
Mechanism Brief Links
Visualizations
Risk Shift by Exposure Stratum
Population-level data only — does not predict individual risk
Tissue Relevance
References
- 1.Tsoi LC, et al. (2017). Psoriasis genome-wide association study. Nature Communications. doi:10.1038/s41467-017-01978-8
- 2.Armstrong AW, et al. (2021). Environmental triggers in psoriasis. JAMA Dermatology. doi:10.1001/jamadermatol.2020.4838