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An Update on the Pathophysiology of Atopic Dermatitis
Kunal Malik1, Kerry D Heitmiller2, Tali Czarnowicki3
1Department of Dermatology, Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, New York, NY 10029, USA; Laboratory of Investigative Dermatology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA; SUNY Downstate College of Medicine, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.
Abstract:
Atopic dermatitis (AD) is increasingly recognized as a complex, inflammatory skin disease involving interplay of multiple elements. This article notes key advances in understanding of immune dysregulation, skin barrier dysfunction, environmental, genetic, and microbial influences orchestrating disease pathogenesis, and the relevance of therapeutic interventions in each area. Accumulating evidence and the discovery of new T-cell subsets has matured AD as a multiple-cytokine-axes-driven disorder, evolved from the widely held belief of it being a biphasic Th1/Th2 disease. These new insights have led to active trials testing multiple, targeted therapeutics with better efficacy and safety-profiles.
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