Abstract

Atopic dermatitis is the most common chronic inflammatory skin disease. Its pathogenesis combines barrier defects, immune dysregulation, and increased skin infections; however, the relative contribution of each of these components is yet to be determined. Uninvolved atopic dermatitis skin also displays broad immune and barrier abnormalities, which highlights a role for proactive treatment strategy. The residual disease genomic profile that accompanies clinical resolution provides further support for proactive treatment approaches. Although intrinsic and extrinsic atopic dermatitis subtypes share a common clinical phenotype, they show some important differences in their Th22/Th17 cytokine profile, which opens the door for personalized specific therapeutics for each disease category.

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