A Psoriasis Gene Emerges

IL-36–Receptor Antagonist Deficiency Causes Generalized Pustular Psoriasis

Kenneth Y. Tsai, MD, PhD

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The long search for psoriasis susceptibility genes has pointed to variants at several genetic loci that are overrepresented in people with psoriasis vulgaris. This first, well-characterized, single-gene mutation to be directly implicated in psoriasis presents a potential target for intervention. Increased interleukin-8 expression is relevant in psoriasis because this cytokine recruits neutrophils, which have a role in the pathogenesis of psoriasis. The inability to dampen innate immune responses may explain why infections trigger flares. Presence of plaque psoriasis in patients with generalized pustular psoriasis suggests that dysregulation of IL-36 signaling may be involved in the more common psoriasis variants and, combined with overexpression of antimicrobial peptides, may explain alterations in the microbiological environment of psoriatic lesions.

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