The pathomechanism of psoriasis involves which cytokine axis as the central driver of keratinocyte hyperproliferation and plaque formation, making it the target of modern biologics?
- A IL-2 and IL-10 axis
- B IL-4 and IL-13 Th2 axis
- C TNF-alpha → IL-23 → IL-17 axis ✓
- D IL-1beta and IL-6 inflammasome axis
Explanation
Psoriasis pathogenesis centres on the TNF-alpha → IL-23 → IL-17 axis: plasmacytoid DCs activated by self-DNA produce TNF-alpha and IFN-alpha; myeloid DCs produce IL-23 which drives Th17 differentiation; IL-17A (and IL-17F) produced by Th17 cells stimulate keratinocytes to proliferate and produce antimicrobial peptides, chemokines, and pro-inflammatory cytokines, perpetuating the cycle. This explains the efficacy of TNF-alpha inhibitors (adalimumab), anti-IL-23 (guselkumab, risankizumab), and anti-IL-17 (secukinumab, ixekizumab). The Th2 (IL-4/IL-13) axis drives atopic dermatitis.
Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.