Content » Vol 100, 100-year theme: Psoriasis (Jan)


The Woronoff Ring in Psoriasis and the Mechanisms of Postinflammatory Hypopigmentation

Jörg C. Prinz
DOI: 10.2340/00015555-3385


The Woronoff ring is a ring-like hypopigmentation zone around regressing psoriasis lesions. Although it was first described more than 100 years ago, its aetiology has remained a mystery. Recent insights into the pathogenesis of psoriasis can now explain the origin of the Woronoff ring. Psoriasis involves an HLA-class I-restricted autoimmune response of CD8+ T cells against melanocytes in the epidermis. The pathogenic CD8+ T cells are not cytotoxic, but are characterized by the production of interleukin-17, interleukin-22 and tumour necrosis factor-α. Interleukin-17 and tumour necrosis factor-α act synergistically on melanocytes by increasing proliferation while inhibiting melanogenesis. This reduces the cellular melanin content despite an increased number of melanocytes in psoriatic lesions. As a consequence, during healing the prior influence of interleukin-17 and tumour necrosis factor-α, despite the increased density of melanocytes, leaves a hypopigmented zone at the edge of regressing psoriasis lesions, which becomes visible as the Woronoff ring. This mechanism can explain a long-discussed puzzling phenomenon in dermatology.


The Woronoff ring is a depigmented zone arising around healing psoriasis plaques. Analysed in detail for the first time approximately 100 years ago, our current understanding of the pathogenesis of psoriasis enables its explanation due to the cytokine pattern of the T-cell-mediated pathogenic melanocyte-specific psoriatic autoimmune response. The production of interleukin-17 and tumour necrosis factor-α causes suppression of melanin synthesis with a simultaneous increase in melanocyte proliferation. This results in an inflammation-induced hypopigmentation surrounding the healing psoriasis lesions. The emergence of the phenomenon is thus coherently integrated into our immunological understanding of psoriatic pathogenesis.

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