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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Curdin Conrad & Jeremy Di Domizio & Alessio Mylonas & Cyrine Belkhodja & Olivier Demaria & Alexander A. Navarini & Anne-Karine Lapointe & Lars E. French & Maxime Vernez & Michel Gilliet, 2018. "TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis," Nature Communications, Nature, vol. 9(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02466-4
    DOI: 10.1038/s41467-017-02466-4
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    Cited by:

    1. Xiangyu Lu & Le Kuai & Fang Huang & Jingsi Jiang & Jiankun Song & Yiqiong Liu & Si Chen & Lijie Mao & Wei Peng & Ying Luo & Yongyong Li & Haiqing Dong & Bin Li & Jianlin Shi, 2023. "Single-atom catalysts-based catalytic ROS clearance for efficient psoriasis treatment and relapse prevention via restoring ESR1," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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