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

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 approach. 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.