Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis.

Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis.
Acta Derm Venereol. 2017 Oct 02;:
Authors: Furue K, Yamamura K, Tsuji G, Mitoma C, Uchi H, Nakahara T, Kido-Nakahara M, Kadono T, Furue M
Abstract
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-α)/ 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-α/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-36α, IL-36β, IL-36γ) 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-α/IL-23/IL-17/IL-22 axis and the functional activation of IL-36R in the epidermal milieu.
PMID: 28967976 [PubMed - as supplied by publisher]

Source: Acta Dermato-Venereologica - October 2, 2017 Category: Dermatology Authors: Furue K, Yamamura K, Tsuji G, Mitoma C, Uchi H, Nakahara T, Kido-Nakahara M, Kadono T, Furue M Tags: Acta Derm Venereol Source Type: research