Abstract
Atopic Dermatitis (AD) is one of the most common chronic inflammatory skin conditions in the developed world. It has a complex aetiology with genetic, immunological and environmental factors causing skin barrier disruption and immune dysregulation (Elias and Steinhoff, 2008). Available immune modulating treatments for AD have proven the importance of Th2 immune activation/dysregulation in AD pathogenesis. In contrast, loss-of-function mutations in the gene encoding filaggrin (FLG) is the strongest genetic pre-disposing factor for development of AD, emphasizing the involvement of skin barrier dysregulation in AD pathogenesis.
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