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. 2019 Oct 9;10:2342. doi: 10.3389/fimmu.2019.02342

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Copyright © 2019 Howell, Kuo and Smith.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Immunopathogenesis of atopic dermatitis. Allergen entry through the disrupted epidermal barrier stimulates keratinocytes to express cytokines, such as IL-33 and TSLP, which trigger ILC2 and Th2 cell mediated inflammation. Skin-resident dendritic cells take up exogenous and self-antigens released from damaged cells and promote type 2 immunity. CD8+ T cells infiltrate atopic dermatitis skin and activate Th2 cells to further release IL-4 and IL-13, which promotes IgE class switching. Cytokines released from skin infiltrating Th17 and Th22 lymphocytes synergize, leading to further barrier impairment and epidermal hyperplasia. DC, dendritic cell; FLG, Filaggrin; Ig, immunoglobulin; IL, interleukin; ILC2, type 2 innate lymphoid cells; INV, Involucrin; LC, Langerhans cell; LOR, Loricrin; OSM, Oncostatin M; OSMRβ, Oncostatin M receptor β; Th, T helper; TSLP, thymic stromal lymphopoietin.