Atopic dermatitis (AD) is characterized by skin barrier defects and increased interleukin (IL)-4/IL-13 expression. Recent evidence also suggests the involvement of innate immunity including Toll-like receptors, IL-33, IL-25, and innate lymphoid cells in the pathogenesis of AD. This article reviews these innate immune components and how they may become an integral part of prognostic factors and therapeutic targets in the treatment of AD.