Differential Epidermal and Dermal Expression of Human ß-Defensin-3 in Paired Lesional and Non-Lesional Psoriatic Skin.

Authors

Fatima Zahra Elfatoiki, Imane Tabyaoui, Farida Marnissi, Latifa Badre, Zineb Serhier, Mohammed Bennani Othmani, Soumiya Chiheb, Hassan Fellah, Nadia Tahiri Jouti

Published in

Dermatology (Basel, Switzerland). Pages 1. Sep 07, 2026. Epub Sep 07, 2026.

Abstract

Psoriasis is a chronic immune-mediated skin disorder characterized by both epidermal hyperproliferation and sustained inflammation. Despite disrupted skin barrier function, psoriatic plaques are rarely associated with infections, a resistance largely attributed to the overexpression of antimicrobial peptides (AMPs), including human β-defensin-3 (hBD-3), a key effector of the innate immune response.
This study aimed to evaluate and compare the expression profile of hBD-3 in lesional and non-lesional skin of Moroccan psoriatic patients.
A cross-sectional study was conducted on 33 patients with plaque psoriasis. hBD-3 expression was evaluated by immunohistochemistry using a semi-quantitative approch. Comparative analyses were performed, to assess epidermal layer expression (ELE) and dermal lymphocytic infiltration (DIL).
Approximately 86.7% of lesional psoriatic samples showed hBD-3 ELE throughout all epidermal layers, whereas in healthy skin, hBD-3 expression was predominantly detected (82.8%) in all layers except the stratum corneum. Moderate to strong hBD-3-positive DIL characterized lesional sites, whereas non-lesional dermis showed predominantly weak or absent DIL. The paired McNemar-Bowker test revealed a significantly higher epidermal (p < 0.0001) and dermal (p = 0.0034) immunohistochemical expression of hBD-3 in lesioned areas compared to healthy skin.
Our findings confirm the overexpression of hBD-3 in lesional skin and reveal, for the first time, to the best of our knowledge, its significant presence in dermal lymphocytes, as a result of the inflammatory microenvironment of psoriatic disease.

PMID:
42704748
Bibliographic data and abstract were imported from PubMed on 08 Sep 2026.

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