IL-23 Kicks Off the Psoriatic Cascade
Dendritic cell IL-23 primes Th17 cells that drive plaque formation.
- IL-23: Key cytokine (p19/p40 heterodimer)
- Th17: Cell type (primed by dendritic cells)
- Dermis: Skin layer (inflammatory infiltrate)
- Chronic: Onset (relapsing autoimmune loop)
Upstream cytokine priming
Short placeholder: IL-23 links innate signals to adaptive Th17 expansion.
IL-17 Drives Keratinocyte Overgrowth
IL-17A signals keratinocytes to proliferate and thicken skin plaques.
- IL-17A: Key cytokine (released by Th17 cells)
- Keratinocyte: Target cell (epidermal hyperproliferation)
- Plaques: Result (scaly, thickened skin)
- Positive: Feedback (amplifies inflammation loop)
Effector cytokine action
Short placeholder: IL-17A pushes keratinocytes into rapid turnover.
Three Biologics, Two Molecular Targets
Skyrizi blocks IL-23; Cosentyx and Taltz block IL-17A directly.
- IL-23 p19: Skyrizi target (risankizumab)
- IL-17A: Cosentyx target (secukinumab)
- IL-17A: Taltz target (ixekizumab)
- Subcutaneous: Dosing (maintenance injections)
Mechanism comparison
Short placeholder: upstream blockade vs direct cytokine neutralization.
Plaques Thin Across the Treatment Course
Weekly progress shows plaques fading as cytokine signaling drops.
- Partial: Week 4 (early clearance visible)
- Marked: Week 8 (majority of plaques fading)
- Near-clear: Week 16 (best-response plateau)
- Varies: Onset speed (by drug class chosen)
Time-course dynamics
Short placeholder: clearance follows a saturating exponential curve.
PASI-75/90/100 Response Buckets
Outcomes are classified by percent improvement from baseline PASI.
- ≥75%: PASI 75 (standard trial endpoint)
- ≥90%: PASI 90 (high-bar response)
- 100%: PASI 100 (complete skin clearance)
- High: Reported rates (for modern biologics)
Response classification
Short placeholder: higher PASI thresholds mean cleaner skin outcomes.
Short placeholder: most patients on these biologics reach PASI 90.