抄録
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.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 5-13 |
| ページ数 | 9 |
| ジャーナル | Acta Dermato-Venereologica |
| 巻 | 98 |
| 発行部数 | 1 |
| DOI | |
| 出版物ステータス | 出版済み - 1 1 2018 |
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All Science Journal Classification (ASJC) codes
- Dermatology
これを引用
Highlighting interleukin-36 signalling in plaque psoriasis and pustular psoriasis. / Furue, Kazuhisa; Yamamura, Kazuhiko; Tsuji, Gaku; Mitoma, Chikage; Uchi, Hiroshi; Nakahara, Takeshi; Kido-Nakahara, Makiko; Kadono, Takafumi; Furue, Masutaka.
：: Acta Dermato-Venereologica, 巻 98, 番号 1, 01.01.2018, p. 5-13.研究成果: ジャーナルへの寄稿 › 評論記事
}
TY - JOUR
T1 - Highlighting interleukin-36 signalling in plaque psoriasis and pustular psoriasis
AU - Furue, Kazuhisa
AU - Yamamura, Kazuhiko
AU - Tsuji, Gaku
AU - Mitoma, Chikage
AU - Uchi, Hiroshi
AU - Nakahara, Takeshi
AU - Kido-Nakahara, Makiko
AU - Kadono, Takafumi
AU - Furue, Masutaka
PY - 2018/1/1
Y1 - 2018/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85041777498&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85041777498&partnerID=8YFLogxK
U2 - 10.2340/00015555-2808
DO - 10.2340/00015555-2808
M3 - Review article
C2 - 28967976
AN - SCOPUS:85041777498
VL - 98
SP - 5
EP - 13
JO - Acta Dermato-Venereologica
JF - Acta Dermato-Venereologica
SN - 0001-5555
IS - 1
ER -