Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis

• Main Authors: Kazuhisa Furue (Author), Kazuhiko Yamamura (Author), Gaku Tsuji (Author), Chikage Mitoma (Author), Hiroshi Uchi (Author), Takeshi Nakahara (Author), Makiko Kido-Nakahara (Author), Takafumi Kadono (Author), Masutaka Furue (Author)
• Format: Book
• Published: Medical Journals Sweden, 2017-10-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Plaque psoriasis and pustular psoriasis are overlapping, but distinct, disorders. The therapeutic response to biologics supports the pivotal role of the tumour necrosis alpha (TNF-?)/ interleukin (IL)-23/IL-17/IL-22 axis in the pathogenesis of these disorders. Recently, functional activation of the IL-36 receptor (IL-36R) was discovered to be another driving force in the pathogenesis of psoriasis. This was first highlighted by the discovery that a loss-of-function mutation of the IL-36R antagonist (IL-36Ra) causes pustular psoriasis. Although the TNF-?/IL-23/IL-17/IL-22 axis and the functional activation of IL-36R are fundamentally involved in plaque psoriasis and pustular psoriasis, respectively, the 2 pathways are closely related and mutually reinforced, resulting in full-blown clinical manifestations. This review summarizes current topics on how IL-36 agonists (IL-36?, IL-36?, IL-36?) signal IL-36R, the pathological expression of IL-36 agonists and IL-36Ra in plaque and pustular psoriatic lesions, and the cross-talk between the TNF-?/IL-23/IL-17/IL-22 axis and the functional activation of IL-36R in the epidermal milieu.

Item Description

0001-5555
1651-2057
10.2340/00015555-2808