アトピー性皮膚炎の発症機序2020

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  • 古江 増隆
    九州大学病院油症ダイオキシン研究診療センター 九州大学大学院医学研究院皮膚科学分野

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タイトル別名
  • Pathogenesis of Atopic Dermatitis 2020
  • アトピーセイ ヒフエン ノ ハッショウ キジョ 2020

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抄録

Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction and chronic pruritus. Excellent clinical efficacy of the anti-interleukin-4 (IL-4) receptor α antibody dupilumab underpins the pivotal roles of T helper type 2 (Th2) cytokines IL-13 and IL-4 in the pathogenesis of AD. Th2 cells also produce IL-31 which is the most important pruritogenic cytokine in AD. IL-13 and IL-4 downregulate the expression of filaggrin in keratinocytes and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce large amounts of thymic stromal lymphopoietin, IL-25 and IL-33, which contribute to Th2 immune deviation via OX40L/OX40 signaling. IL-13 and IL-4 also amplify the IL-31-mediated pruritus. In this review, I summarize recent advances in the pathogenesis of AD.

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