Abstract
Atopic dermatitis (AD) is a common inflammatory skin disease with a complex pathophysiology, intertwining immune dysregulation, epidermal barrier dysfunction, IgE sensitization, environmental factors and genetic predisposition. It has been recently identified that interleukins -4 and -13 play crucial roles in the type-2-driven inflammation that characterizes AD, contributing to its symptomatology. Novel therapeutic approaches that target Th2 cytokines and their respective pathways have been developed, aiming to optimize the treatment of AD.