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Atopic Dermatitis and Type 2 Immune Deviation

  • Urticaria and Atopic Dermatitis (M Furue and T Nakahara, Section Editors)
  • Published:
Current Treatment Options in Allergy Aims and scope Submit manuscript

Abstract

Purpose of the review

To summarize recent topics on type 2 signatures in atopic dermatitis (AD).

Recent findings

Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal.

Summary

Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD.

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Correspondence to Masutaka Furue M.D., Ph.D..

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Furue, M., Ulzii, D., Vu, Y.H. et al. Atopic Dermatitis and Type 2 Immune Deviation. Curr Treat Options Allergy 6, 200–210 (2019). https://doi.org/10.1007/s40521-019-00219-w

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