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  1. C100 医学部/医学系研究科
  2. C100a 雑誌掲載論文
  3. 学術雑誌

Pustular psoriasis as an autoinflammatory keratinization disease (AiKD): Genetic predisposing factors and promising therapeutic targets

http://hdl.handle.net/2237/0002002689
http://hdl.handle.net/2237/0002002689
56e37f70-5dfa-4388-bf7d-3509d328a05b
名前 / ファイル ライセンス アクション
draft_Proof_hi.pdf draft_Proof_hi.pdf (972 KB)
Item type itemtype_ver1(1)
公開日 2022-05-09
タイトル
タイトル Pustular psoriasis as an autoinflammatory keratinization disease (AiKD): Genetic predisposing factors and promising therapeutic targets
言語 en
著者 Akiyama, Masashi

× Akiyama, Masashi

en Akiyama, Masashi

Search repository
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利
言語 en
権利情報 © 2022. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
キーワード
主題Scheme Other
主題 AP1S3
キーワード
主題Scheme Other
主題 CARD14
キーワード
主題Scheme Other
主題 IL-36
キーワード
主題Scheme Other
主題 IL36RN
キーワード
主題Scheme Other
主題 MPO
キーワード
主題Scheme Other
主題 SERPINA3
内容記述
内容記述 Pustular psoriasis is a chronic inflammatory skin disease characterized by erythematous plaques with sterile pustules. It includes the distinct clinical entities generalized pustular psoriasis (GPP), acrodermatitis continua of Hallopeau (ACH) and palmoplantar pustular psoriasis (PPPP). Recently clarified pathomechanisms of pustular psoriasis indicate that hyperactivation of the skin innate immunity, including of the IL-1/IL-36 axis, plays an important role in the pathogenesis of pustular psoriasis. Autoinflammatory keratinization disease (AiKD) is the umbrella clinical entity for inflammatory keratinization disorders with genetic autoinflammatory pathomechanisms, and pustular psoriasis is a representative AiKD. To date, mutations/variants in five genes—IL36RN, CARD14, AP1S3, MPO and SERPINA3—have been reported to be genetic causative or predisposing factors for pustular psoriasis. The pathogenic mechanisms induced by the mutations/variants in these genes are all closely related to the excessive activation of skin innate immunity and autoinflammation. A number of biologics (e.g., tumor necrosis factor inhibitors, IL-17/IL-17 receptor inhibitors and IL-23 inhibitors) and granulocyte and monocyte adsorption apheresis are used to treat pustular psoriasis. Recently, based on novel information on the pathomechanisms of pustular psoriasis, which are mainly associated with autoinflammation, inhibitors of several pathogenic pathways, including of the IL-1, IL-36, IL-8 and granulocyte colony-stimulating factor signaling pathways, have been studied as emerging treatments.
言語 en
内容記述タイプ Abstract
出版者
言語 en
出版者 Elsevier
言語
言語 eng
資源タイプ
資源タイプresource http://purl.org/coar/resource_type/c_6501
タイプ journal article
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
関連情報
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1016/j.jdermsci.2021.11.009
収録物識別子
収録物識別子タイプ PISSN
収録物識別子 0923-1811
書誌情報 en : Journal of Dermatological Science

巻 105, 号 1, p. 11-17, 発行日 2022-01
ファイル公開日
日付 2023-01-01
日付タイプ Available
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