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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

Toll-like receptor 4 antagonist TAK-242 inhibits autoinflammatory symptoms in DITRA

http://hdl.handle.net/2237/26851
7d686741-9564-4ae0-9d2e-9c974fe63189
名前 / ファイル ライセンス アクション
Shibata_et_al_J_Autoimmun.pdf Shibata_et_al_J_Autoimmun.pdf ファイル公開:2018/06/01 (4.0 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-08-01
タイトル
タイトル Toll-like receptor 4 antagonist TAK-242 inhibits autoinflammatory symptoms in DITRA
著者 Shibata, Akitaka

× Shibata, Akitaka

WEKO 72926

Shibata, Akitaka

Search repository
Sugiura, Kazumitsu

× Sugiura, Kazumitsu

WEKO 72927

Sugiura, Kazumitsu

Search repository
Furuta, Yasuhide

× Furuta, Yasuhide

WEKO 72928

Furuta, Yasuhide

Search repository
Mukumoto, Yoshiko

× Mukumoto, Yoshiko

WEKO 72929

Mukumoto, Yoshiko

Search repository
Kaminuma, Osamu

× Kaminuma, Osamu

WEKO 72930

Kaminuma, Osamu

Search repository
Akiyama, Masashi

× Akiyama, Masashi

WEKO 72931

Akiyama, Masashi

Search repository
権利
権利情報 © 2017. 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 Autoinflammation
キーワード
主題Scheme Other
主題 Deficiency of IL-36 receptor antagonist
キーワード
主題Scheme Other
主題 Generalized pustular psoriasis
キーワード
主題Scheme Other
主題 Toll-like receptor 4
キーワード
主題Scheme Other
主題 LPS
キーワード
主題Scheme Other
主題 TAK-242
抄録
内容記述 Background: IL36RN encodes the IL-36 receptor antagonist (IL-36Ra), and loss-of-function mutations in IL36RN define a recessively inherited autoinflammatory disease named “deficiency of IL-36Ra” (DITRA). DITRA causes systemic autoinflammatory diseases, including generalized pustular psoriasis (GPP), an occasionally life-threatening disease that is characterized by widespread sterile pustules on the skin, fever and other systemic symptoms. GPP can present at any age, and provocative factors include various infections, medicines and pregnancy. Objective: We aimed to elucidate the role of toll-like receptor 4 (TLR4) signaling in DITRA and to innovate an efficient treatment for DITRA. Methods: We generated Il36rn−/− mice and treated them with TLR4 agonist to establish DITRA model mice. Furthermore, we administrated TLR4 antagonist TAK-242 to the model mice to inhibit the DITRA symptoms. Result: Il36rn−/− mice treated by TLR4 agonist showed autoinflammatory symptoms in skin, articulation and liver. Thus, we established model mice for DITRA or GPP that show cutaneous, articular, and hepatic autoinflammatory symptoms typical of DITRA or GPP: sterile pustules on the skin, liver abscesses and enthesitis of the hind paws. Additionally, these symptoms were canceled by TAK-242 administration. We demonstrated the inhibitory effects of the TLR4 antagonist TAK-242 on the autoinflammatory symptoms exhibited by the DITRA models. Conclusion: We suggested that blockage of TLR4 signaling is a promising treatment for DITRA and GPP.
内容記述タイプ Abstract
出版者
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
ISSN
収録物識別子タイプ ISSN
収録物識別子 0896-8411
書誌情報 Journal of Autoimmunity

巻 80, p. 28-38, 発行日 2017-06
著者版フラグ
値 author
URI
識別子 https://doi.org/10.1016/j.jaut.2017.01.007
識別子タイプ DOI
URI
識別子 http://hdl.handle.net/2237/26851
識別子タイプ HDL
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