アトピー性皮膚炎治療の新時代 : 病態解明の進歩と新規治療薬の開発
デジタルデータあり（九州大学学術情報リポジトリ(QIR)）
すぐに読む
学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
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- 資料種別
- 記事
- 著者・編者
- 中原 剛士
- 著者標目
- 並列タイトル等
- New Era of Therapeutics in Atopic Dermatitis
- タイトル（掲載誌）
- 福岡医学雑誌 = Fukuoka acta medica
- 巻号年月日等（掲載誌）
- 113(3)=1172:2022.9.25
- 掲載巻
- 113
- 掲載号
- 3
- 掲載通号
- 1172
- 掲載ページ
- 45-52
- 掲載年月日（W3CDTF）
- 2022-09-25
- ISSN（掲載誌）
- 0016-254X
- ISSN-L（掲載誌）
- 0016-254X
- 出版事項（掲載誌）
- 福岡 : 福岡医学会
- 出版地（国名コード）
- JP
- 本文の言語コード
- jpn
- NDLC
- 対象利用者
- 一般
- 所蔵機関
- 国立国会図書館
- 請求記号
- Z19-86
- 連携機関・データベース
- 国立国会図書館 : 国立国会図書館雑誌記事索引
- 書誌ID（NDLBibID）
- 032763024
- 整理区分コード
- 632
- 要約等
- Atopic dermatitis is a common, chronic inflammatory skin disease that is characterized by skin barrier dysfunction, inflammation and intense itch. Although the exact mechanisms behind its pathogenesis remain unclear, it is evident that the complex interplay among barrier dysfunction, inflammation and itch are critical in its development, progression and chronicity. Barrier-disrupted skin produces thymic stromal lymphopoietin and interleukin (IL)-33 ; these in turn promote skin inflammation characterized by type 2 immune deviation. This inflammation then downregulates the expression of filaggrin in keratinocytes and exacerbates epidermal barrier dysfunction. Furthermore, various itch mediators/pruritogens produced during this inflammatory process can act directly on sensory nerves and cause itch. Based on this understanding of the pathophysiology, many new drugs are being developed, and a new era of treatment is underway. Specifically, anti-IL-4 receptor antibody, anti-IL-31 receptor antibody, and JAK inhibitors are already available for use in clinical practice. Still, however, how to select the optimal drug remains a major challenge. In this review, we summarize the basics and recent advances in our understanding of the pathophysiology of atopic dermatitis, including our recent research findings. In addition, the status of development of new drugs is also outlined.
- DOI
- 10.15017/6770310
- オンライン閲覧公開範囲
- インターネット公開
- 掲載誌（NCID）
- AN00215478
- 連携機関・データベース
- 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
- 提供元機関・データベース
- 九州大学学術情報リポジトリ(QIR)
- 要約等
- Atopic dermatitis is a common, chronic inflammatory skin disease that is characterized by skin barrier dysfunction, inflammation and intense itch. Although the exact mechanisms behind its pathogenesis remain unclear, it is evident that the complex interplay among barrier dysfunction, inflammation and itch are critical in its development, progression and chronicity. Barrier-disrupted skin produces thymic stromal lymphopoietin and interleukin (IL)-33 ; these in turn promote skin inflammation characterized by type 2 immune deviation. This inflammation then downregulates the expression of filaggrin in keratinocytes and exacerbates epidermal barrier dysfunction. Furthermore, various itch mediators/pruritogens produced during this inflammatory process can act directly on sensory nerves and cause itch. Based on this understanding of the pathophysiology, many new drugs are being developed, and a new era of treatment is underway. Specifically, anti-IL-4 receptor antibody, anti-IL-31 receptor antibody, and JAK inhibitors are already available for use in clinical practice. Still, however, how to select the optimal drug remains a major challenge. In this review, we summarize the basics and recent advances in our understanding of the pathophysiology of atopic dermatitis, including our recent research findings. In addition, the status of development of new drugs is also outlined.
- DOI
- 10.15017/6770310
- オンライン閲覧公開範囲
- インターネット公開
- 関連情報（URI）
- 連携機関・データベース
- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
- Japan Link Center学術機関リポジトリデータベース雑誌記事索引データベース
- 書誌ID（NDLBibID）
- 032763024