Abstract

Atopic dermatitis (AD) is a common and relapsing skin disease that is characterized by skin barrier dysfunction, inflammation, and chronic pruritus. While AD was previously thought to occur primarily in children, increasing evidence suggests that AD is more common in adults than previously assumed. Accumulating evidence from experimental, genetic, and clinical studies indicates that AD expression is a precondition for the later development of other atopic diseases, such as asthma, food allergies, and allergic rhinitis. Although the exact mechanisms of the disease pathogenesis remain unclear, it is evident that both cutaneous barrier dysfunction and immune dysregulation are critical etiologies of AD pathology. This review explores recent findings on AD and the possible underlying mechanisms involved in its pathogenesis, which is characterized by dysregulation of immunological and skin barrier integrity and function, supporting the idea that AD is a systemic disease. These findings provide further insights for therapeutic developments aiming to repair the skin barrier and decrease inflammation.

Highlights

  • Atopic dermatitis (AD) is a common chronic relapsing inflammatory skin disease that repeatedly passes through the following stages: exacerbation and improvement

  • Innate lymphoid cells (ILCs) in the skin are activated by TSLP, IL-33, and IL-25, which are highly expressed in atopic dermatitis

  • These findings suggest a critical role of ILC2s in allergic skin diseases, such as atopic dermatitis

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Summary

Introduction

Atopic dermatitis (AD) is a common chronic relapsing inflammatory skin disease that repeatedly passes through the following stages: exacerbation and improvement. AD manifests as severe pruritus, distinct shapes and distributions of skin lesions, and genetic factors that show a personal or familial history of atopic diseases. AD has a complex etiology including genetic, immunological, and environmental factors that cause skin barrier abnormalities and immune dysfunctions (Figure 1), which are considered crucial to the pathogenesis of AD [3]. Major contributors to the pathogenesis of skin barrier abnormalities in AD include decreased filaggrin, ceramides, and antimicrobial peptides; increased serine protease (SP); decreased. Keratinocyte proliferation is restricted to the basal cell layers. 3. Skin Barrier Abnormalities in Atopic Dermatitis AccumulatFiniggureev2id. Sci. 2020, 21, 2867 has been demonstrated in AD patients [14,15], and these molecules are expected to affect permeability barrier homeostasis

Lipids
Filaggrin
Toll-Like Receptors and Atopic Dermatitis
The Emerging Role of Inflammasomes in Atopic Dermatitis Symptoms
Crosstalk between the Skin Barrier and Immune System in Atopic Dermatitis
Findings
11. Conclusions
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