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Immunology of Psoriatic Disease

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Front. Immunol. | doi: 10.3389/fimmu.2018.02746

Psoriasis: Classical versus Paradoxical: The Yin Yang of TNF and Type I Interferon

  • 1Dermatology, Lausanne University Hospital (CHUV), Switzerland
  • 2Département de dermatologie et vénéréologie, Hôpital Universitaire de Lausanne (CHUV), Switzerland

Chronic plaque psoriasis is a common debilitating skin disease. The identification of the pathogenic role of the TNF/IL-23/TH17 pathway has enabled the development of targeted therapies used in the clinic today. Anti-TNF agents have become a benchmark for the treatment of numerous chronic inflammatory diseases such as psoriasis. Although being highly effective in psoriasis treatment, anti-TNFs can themselves induce psoriasis-like skin lesions, a side effect called paradoxical psoriasis. In this review, we provide a comprehensive look at the different cellular and molecular players involved in classical plaque psoriasis and contrast its pathogenesis to paradoxical psoriasis, which is clinically similar but immunologically distinct. Classical psoriasis is a T-cell mediated autoimmune disease driven by TNF, characterized by T cell memory and a relapsing disease course. In contrast, paradoxical psoriasis is caused by the absence of TNF and represents an ongoing IFNα-driven innate inflammation that fails to elicit T-cell autoimmunity and lacks memory T cell-mediated relapses.

Keywords: Plaque psoriasis, paradoxical psoriasis, TNF, IL-23, Th17, Type I interferon (IFN)

Received: 17 Aug 2018; Accepted: 07 Nov 2018.

Edited by:

Eva Reali, Istituto Ortopedico Galeazzi (IRCCS), Italy

Reviewed by:

Yumin Xia, Second Affiliated Hospital of Xi'an Jiaotong University, China
Silvia Vidal, Sant Pau Institute for Biomedical Research, Spain  

Copyright: © 2018 Conrad and Mylonas. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Curdin Conrad, Lausanne University Hospital (CHUV), Dermatology, Lausanne, 1011, Switzerland,