Atopic dermatitis: immune deviation, barrier dysfunction, IgE autoreactivity and new therapies

DOI Web Site Web Site 被引用文献25件 参考文献113件
  • Furue Masutaka
    Department of Dermatology, Kyushu University Research and Clinical Center for Yusho and Dioxin, Kyushu University Division of Skin Surface Sensing, Department of Dermatology, Kyushu University
  • Chiba Takahito
    Department of Dermatology, Kyushu University
  • Tsuji Gaku
    Department of Dermatology, Kyushu University Research and Clinical Center for Yusho and Dioxin, Kyushu University
  • Ulzii Dugarmaa
    Department of Dermatology, Kyushu University
  • Kido-Nakahara Makiko
    Department of Dermatology, Kyushu University
  • Nakahara Takeshi
    Department of Dermatology, Kyushu University Division of Skin Surface Sensing, Department of Dermatology, Kyushu University
  • Kadono Takafumi
    Department of Dermatology, St. Marianna University School of Medicine

この論文をさがす

説明

<p>Atopic dermatitis (AD) is a chronic or chronically relapsing, eczematous, severely pruritic skin disorder mostly associated with IgE elevation and skin barrier dysfunction due to decreased filaggrin expression. The lesional skin of AD exhibits Th2- and Th22-deviated immune reactions that are progressive during disease chronicity. Th2 and Th22 cytokines further deteriorate the skin barrier by inhibiting filaggrin expression. Some IgEs are reactive to self-antigens. The IgE autoreactivity may precipitate the chronicity of AD. Upon activation of the ORAI1 calcium channel, atopic epidermis releases large amounts of thymic stromal lymphopoietin (TSLP), which initiates the Th2 and Th22 immune response. Th2-derived interleukin-31 and TSLP induce an itch sensation. Taken together, TSLP/Th2/Th22 pathway is a promising target for developing new therapeutics for AD. Enhancing filaggrin expression using ligands for the aryl hydrocarbon receptor may also be an adjunctive measure to restore the disrupted barrier function specifically for AD.</p>

収録刊行物

被引用文献 (25)*注記

もっと見る

参考文献 (113)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ