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Atopic dermatitis

Abstract

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, with a lifetime prevalence of up to 20% and substantial effects on quality of life. AD is characterized by intense itch, recurrent eczematous lesions and a fluctuating course. AD has a strong heritability component and is closely related to and commonly co-occurs with other atopic diseases (such as asthma and allergic rhinitis). Several pathophysiological mechanisms contribute to AD aetiology and clinical manifestations. Impairment of epidermal barrier function, for example, owing to deficiency in the structural protein filaggrin, can promote inflammation and T cell infiltration. The immune response in AD is skewed towards T helper 2 cell-mediated pathways and can in turn favour epidermal barrier disruption. Other contributing factors to AD onset include dysbiosis of the skin microbiota (in particular overgrowth of Staphylococcus aureus), systemic immune responses (including immunoglobulin E (IgE)-mediated sensitization) and neuroinflammation, which is involved in itch. Current treatments for AD include topical moisturizers and anti-inflammatory agents (such as corticosteroids, calcineurin inhibitors and cAMP-specific 3ʹ,5ʹ-cyclic phosphodiesterase 4 (PDE4) inhibitors), phototherapy and systemic immunosuppressants. Translational research has fostered the development of targeted small molecules and biologic therapies, especially for moderate-to-severe disease.

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Fig. 1: Global prevalence of atopic dermatitis symptoms.
Fig. 2: Stage-based pathogenesis and main mechanisms of atopic dermatitis.
Fig. 3: Itch pathways and type 2 immunity cytokine signalling in atopic dermatitis.
Fig. 4: Clinical manifestations of atopic dermatitis.

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Nature Reviews Disease Primers would like to thank M. Furue, S. Ständer, E. Weisshaar and the other anonymous reviewer(s) for their contribution to the peer review of this work.

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Introduction (A.D.I. and S.W.); Epidemiology (S.W.); Mechanisms/pathophysiology (all authors); Diagnosis, screening and prevention (T.B.); Management (L.A.B., T.B., A.D.I. and S.W.); Quality of life (L.A.B.); Outlook (A.D.I. and S.W.); Overview of Primer (A.D.I. and S.W.).

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Correspondence to Stephan Weidinger or Alan D. Irvine.

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Competing interests

S.W. has received honoraria for invited lectures from and served on advisory boards for Galderma, Novartis, Pfizer, Regeneron and Sanofi and has received research funding from La Roche-Posay, Novartis, Pfizer and Sanofi. L.A.B. has received consulting fees from AbbVie, AnaptysBio, Boehringer Ingelheim, Celgene, GlaxoSmithKline, Lilly, Novan, Novartis, Realm Therapeutics, Regeneron and Sanofi-Genzyme; she is principal investigator for clinical trials for AbbVie, Realm Therapeutics and Regeneron and is a stock owner of Medtronic and Pfizer. T.B. has received honoraria for invited lectures from and served on consultant and/or advisory boards for AbbVie, Allmiral, AnaptysBio, Asana Biosciences, Celgene, Daiichi-Sankyo, Dermavant, Galapagos, Galderma, Glenmark, GlaxoSmithKline, Kymab, LEO Pharma, La Roche-Posay, Lilly, L’Oréal, Menlo, Novartis, Pfizer, Roche–Genentech and Sanofi-Genzyme; he was principal investigator for clinical trials with Galderma, LEO Pharma, Lilly, Menlo, Pfizer, Regeneron–Sanofi and Roche–Genentech. K.K. has received honoraria for invited lectures from and served on consultant and/or advisory boards for Chugai, Kyowa Hakko Kirin, LEO Pharma, Mitsubishi Tanabe, Maruho, Pola and Regeneron–Sanof; he was principal investigator for clinical trials with Japan Tobacco, Maruho and Regeneron–Sanofi. A.D.I. has received honoraria for invited lectures from and served on consultant and/or advisory boards for AbbVie, Galderma, Lilly, Novartis, Pfizer, Roche–Genentech and Sanofi-Genzyme; he was principal investigator for clinical trials with AbbVie and Regeneron–Sanofi.

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Weidinger, S., Beck, L.A., Bieber, T. et al. Atopic dermatitis. Nat Rev Dis Primers 4, 1 (2018). https://doi.org/10.1038/s41572-018-0001-z

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