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.
• Notes: 0001-5555; 1651-2057; 10.2340/00015555-2808
• Keywords: psoriasis; pustularpsoriasis; IL-36; IL-36receptor; IL-36receptorantagonist; IL-17; IL-22; Dermatology; RL1-803
• Source: Acta Dermato-Venereologica, Vol 98, Iss 1, Pp 5-13 (2017)

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.