Pathogenesis of Atopic Dermatitis (AD) and the role of allergic factors

A. Cantani

Division of Allergy and Clinical Immunology, Department of Pediatrics, “La Sapienza” University – Rome (Italy)

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• Allergology

Abstract. – Objective. In this paper we will demonstrate that the exact pathogenesis of atopic dermatitis (AD) remains enigmatic, however the central defect is genetically determined, and the several dysfunctions we will highlight all point to a vicious cycle of allergen exposure, allergen-specific IgE production, and chronic Th2 cell stimulation. An important role is played by the late phase of IgE-mediated hypersensitivity, and evidence is accumulating that eosinophils actively participate in late phase-allergic reactions also in the skin. Observations. AD is the first atopic disease to appear in the absolute sense: dendritic cells (DC) develop firstly in the skin and then in lung, in addition to homing receptors for T lymphocytes that are selective for skin localizations and not for lung. Among the DC, a primary role is reserved to Langerhans cells (LC) that express E-cadherin, a homophilic adhesion molecule that is prominently represented in epithelia. In addition keratinocytes and the interleukins (IL) they express are capable of activating a host of IgE-bearing cells. Conclusion. Although much new information regarding the pathogenesis of AD has evolved over the past several years, the basic underlying etiology of this disorder remains elusive. Preventive measures are the only treatment for AD. We hope that the coming years will witness the development of new strategies for the treatment of AD, aimed at specific targets based on a thorough understanding of its pathogenesis.

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