🩹 IL-17/IL-23 Biologic Therapy Simulator

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.