ArticleThe Journal of investigative dermatology2026
Defensins Mediate Skin Inflammation and Itch in Psoriasis.
Article in The Journal of investigative dermatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Psoriasis is an inflammatory skin condition that features marked upregulation of keratinocyte-derived antimicrobial peptides, particularly β-defensins. Yet the functions of these peptides in skin inflammation remain unclear. In this study, we used a Defensin cluster knockout mouse to evaluate the potential roles of defensins as neuroimmune modulators in psoriasis. Deletion of the defensin gene cluster (Def cKO) in keratinocytes significantly attenuated imiquimod-induced psoriatic inflammation, with reduced hyperkeratosis, erythema, scaling, and expression of inflammatory cytokines and chemokines. Additionally, the Def cKO mice exhibited reduced neutrophil and IL-17+ TCRγδ T cell infiltration in the psoriatic skin, indicating a critical role of defensins in amplifying Th17 immunity. Behavioural analysis further revealed that loss of defensins reduced psoriatic itch, and we showed that human β-defensin 2 directly activated small-diameter Mrgpra3 neurons to elicit robust scratching. Overall, our study revealed that β-defensins play an important role in mediating inflammation and itch associated with psoriasis by activating neutrophils, type 17 immune response, and pruriceptive sensory neurons, suggesting defensin signalling as a potential therapeutic target in psoriasis.
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