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Giornale Italiano di Dermatologia e Venereologia 2019 August;154(4):418-24

DOI: 10.23736/S0392-0488.18.06202-8

Copyright © 2018 EDIZIONI MINERVA MEDICA

language: English

Psoriasis and the TNF/IL23/IL17 axis

Kazuhisa FURUE 1, Takamichi ITO 1, Gaku TSUJI 1, Takafumi KADONO 2, Masutaka FURUE 1

1 Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; 2 Department of Dermatology, St. Marianna University School of Medicine, Kawasaki, Japan



The excellent response of psoriasis to anti-TNF-α(TNF)/IL23/IL17A biologics implies a crucial role for the TNF/IL23/IL17 axis in developing psoriasis. In addition to the TNF/IL23/IL17 axis provided by immune cells, current evidence points to an important contribution of TNF, IL23 and IL17C produced from non-hematopoietic keratinocytes. Therefore, crosstalk between immune cells and keratinocytes forms a multilayered feed-forward loop to accelerate the TNF/IL23/IL17A axis. Many biologics have already been licensed or are under clinical trials. Given that the IL-17 signature is more upregulated in the skin than in synovium in psoriatic arthritis, anti-IL-23/IL-17 agents seem to be superior to anti-TNF-α remedies in the treatment of skin lesions. In this review, we summarize recent topics in psoriasis and the TNF/IL23/IL17 axis.


KEY WORDS: Psoriasis; Tumor necrosis factor-alpha; Interleukin-23; Interleukin-17

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