TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis

Curdin Conrad (), Jeremy Di Domizio, Alessio Mylonas, Cyrine Belkhodja, Olivier Demaria, Alexander A. Navarini, Anne-Karine Lapointe, Lars E. French, Maxime Vernez and Michel Gilliet ()
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Curdin Conrad: University Hospital CHUV
Jeremy Di Domizio: University Hospital CHUV
Alessio Mylonas: University Hospital CHUV
Cyrine Belkhodja: University Hospital CHUV
Olivier Demaria: University Hospital CHUV
Alexander A. Navarini: University Hospital of Zurich
Anne-Karine Lapointe: University Hospital CHUV
Lars E. French: University Hospital of Zurich
Maxime Vernez: University Hospital CHUV
Michel Gilliet: University Hospital CHUV

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract Although anti-tumor necrosis factor (TNF) agents are highly effective in the treatment of psoriasis, 2–5% of treated patients develop psoriasis-like skin lesions called paradoxical psoriasis. The pathogenesis of this side effect and its distinction from classical psoriasis remain unknown. Here we show that skin lesions from patients with paradoxical psoriasis are characterized by a selective overexpression of type I interferons, dermal accumulation of plasmacytoid dendritic cells (pDC), and reduced T-cell numbers, when compared to classical psoriasis. Anti-TNF treatment prolongs type I interferon production by pDCs through inhibition of their maturation. The resulting type I interferon overexpression is responsible for the skin phenotype of paradoxical psoriasis, which, unlike classical psoriasis, is independent of T cells. These findings indicate that paradoxical psoriasis represents an ongoing overactive innate inflammatory process, driven by pDC-derived type I interferon that does not lead to T-cell autoimmunity.

Date: 2018
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DOI: 10.1038/s41467-017-02466-4

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