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      Open Access

      Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis

      JID Innovations
      Vol. 2Issue 5100131Published online: April 25, 2022
      • Lisa A. Beck
      • Michael J. Cork
      • Masayuki Amagai
      • Anna De Benedetto
      • Kenji Kabashima
      • Jennifer D. Hamilton
      • and others
      Cited in Scopus: 0
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      Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host–environment interactions involving keratinocytes as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T helper type 2 cells, which produce type 2 cytokines, including IL-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts the expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances Staphylococcus aureus skin colonization.
      Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
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