Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_57A9835FCAA8
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon.
Périodique
Frontiers in immunology
Auteur⸱e⸱s
Mylonas A., Conrad C.
ISSN
1664-3224 (Electronic)
ISSN-L
1664-3224
Statut éditorial
Publié
Date de publication
2018
Peer-reviewed
Oui
Volume
9
Pages
2746
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: epublish
Résumé
Chronic plaque psoriasis is a common debilitating skin disease. The identification of the pathogenic role of the TNF/IL-23/T <sub>H</sub> 17 pathway has enabled the development of targeted therapies used in the clinic today. Particularly, TNF inhibitors 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, characterised by T-cells memory, and a relapsing disease course. In contrast, paradoxical psoriasis is caused by the absence of TNF and represents an ongoing type-I interferon-driven innate inflammation that fails to elicit T-cell autoimmunity and lacks memory T cell-mediated relapses.
Mots-clé
Humans, Immunologic Memory, Interferon Type I/immunology, Interleukin-23/immunology, Psoriasis/immunology, Psoriasis/pathology, Signal Transduction/immunology, Th17 Cells/immunology, Th17 Cells/pathology, Tumor Necrosis Factor-alpha/immunology, IL-23, TH17, TNF, paradoxical psoriasis, plaque psoriasis, type I-interferon
Pubmed
Web of science
Open Access
Oui
Création de la notice
17/12/2018 10:06
Dernière modification de la notice
21/11/2022 9:18
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