Chronic autoimmune disease characterised by well-demarcated, erythematous, scaly plaques

Aetiology

• Genetic predisposition + environmental triggers
  • Associated with specific HLA types
• Equal sex incidence
• Two peaks in incidence - 20s and 50s

Precipitating factors

• Stress
• Trauma
• Alcohol and smoking
• Infection - strep throat
• Drugs - β-blockers, lithium, anti malarial drugs, swift withdrawal of topical or systemic steroids ('rebound' psoriasis)

Pathophysiology

• Triggered by environmental factors in genetically susceptible individuals
  • Bacterial pharyngitis, Koebner phenomenon (mild trauma to skin), interferon therapy, drugs
• Hallmark of skin lesions is inflammation
• Plaques are reversible

1. Keratinocytes under stress (environmental factors) release factors that stimulate plasmacytoid DC to produce IFN⍺, and also release Il-1β/IL-6 and TNF
2. Chemical signals activate DC, which migrate to skin draining lymph node and present to and activate T cells (TH1 and TH17)
3. T cells stimulate an inflammatory cascade in the dermis involving anti-microbial peptide release and neutrophil-attracting chemokines
   1. Complement attracts neutrophils to keratin layer → Munro micro abscesses
4. Results in keratinocyte proliferation