Pathogenesis of Atopic Dermatitis: Current Paradigm

Authors

  • Dugarmaa Ulzii Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan
  • Gaku Tsuji Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan
  • Masutaka Furue Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan
  • Takeshi Nakahara Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan
  • Yen Vu Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan
Abstract:

Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction and chronic pruritus. In this review, recent advances in the pathogenesis of AD are summarized. Clinical efficacy of the anti-IL-4 receptor antibody dupilumab implies that type 2 cytokines IL-4 and IL-13 have pivotal roles in atopic inflammation. The expression of IL-4 and IL-13 as well as type 2 chemokines such as CCL17, CCL22 and CCL26 is increased in the lesional skin of AD. In addition, IL-4 and IL-13 down-regulate 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, conducing to type 2 immune deviation via OX40L/OX40 signaling. IL-31, produced by type 2 T cells, is a cardinal pruritogenic cytokine. IL-4 and IL-13 also amplify the IL-31-mediated sensory nerve signal. These molecules are particularly important targets for future drug development for AD.

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Journal title

volume 16  issue 2

pages  97- 107

publication date 2019-06-01

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