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Psoriasis Pathogenesis — SCE Dermatology MCQ

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ModerateInflammatory DermatosesPsoriasis PathogenesisSCE Dermatology

A 55-year-old man has chronic plaque psoriasis. His dermatologist explains that psoriasis is driven by the IL-23/Th17 immune axis. In simple terms, what is the role of IL-23 in psoriasis pathogenesis?

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Correct answer: A — IL-23 maintains and expands pathogenic Th17 cells that produce IL-17A/F and IL-22, driving keratinocyte proliferation and epidermal inflammation

IL-23 is a master upstream cytokine that maintains and expands pathogenic Th17 cells in psoriasis. IL-23 (composed of p19 + p40 subunits) activates STAT3 signalling in Th17 cells, driving production of downstream effector cytokines: IL-17A, IL-17F (which stimulate keratinocyte proliferation, neutrophil recruitment, and antimicrobial peptide production) and IL-22 (which drives epidermal hyperplasia). This IL-23/Th17 axis is the central pathogenic pathway in psoriasis. The clinical success of IL-23 and IL-17 inhibitors validates this model. Blocking IL-23 upstream provides sustained efficacy with infrequent dosing because it prevents regeneration of the entire pathogenic T-cell population.

Reference: BAD 2020; Psoriasis Immunology Review