Recent advances in atopic dermatitis and psoriasis: Genetic background, barrier function, and therapeutic targets

• Atopic dermatitis (AD) and psoriasis have similar pathological background in common such as barrier dysfunction and enhanced IL-22 expression.
• Th2/Th22-polarized immune status together with an attenuated Th17 axis may cause insufficient induction of antimicrobial peptides and more severe barrier dysfunction in AD.
• Recent advances in AD and psoriasis in terms of genetic background, barrier function, and therapeutic targets may lead to new therapeutic strategies.

Atopic dermatitis (AD) and psoriasis are common inflammatory skin diseases. Although clinical pictures of these two diseases are quite different, they share some common pathological backgrounds such as barrier dysfunction and enhanced IL-22 expression. To explain the clinical differences of the diseases, it has been proposed that Th2/Th22-polarized immune status together with an attenuated Th17 axis may cause insufficient induction of antimicrobial peptides and more severe barrier dysfunction in AD. While skin barrier dysfunction is commonly seen in AD and psoriasis, a Th2-dominant cytokine milieu down-regulates immunity against infections, which are commonly seen in lesional skin of AD. In the era of biologics, increase in the understanding or new discoveries of molecules involved in the development of various diseases will instantly lead to a new therapeutic strategy. In this review, we give an overview of recent advances in AD and psoriasis, especially on genetic background, barrier function, and therapeutic targets.