Atopic dermatitis (AD) presents as a chronic relapsing skin disease with high prevalence in children. The typical distributed skin lesions make the clinical diagnosis of AD very simple and clear-cut in most of the cases. In contrast, the underlying mechanisms leading to the manifestation of AD are more than complex and consist of genetic components combined with various deficiencies on the level of innate and adaptive immune mechanisms. Challenged by this puzzle, scientific approaches of the last years have made considerable progress in gaining insights into the mechanisms, which cause AD. AD is a biphasic inflammatory skin disease characterized by an initial phase predominated by Th2 cytokines which switches into a second, more chronic Th1-dominated eczematous phase. Two different dendritic cell (DC) subtypes bearing the high-affinity receptor for IgE (FcepsilonRI) have been identified in the epidermal skin of AD patients: FcepsilonRIhigh Langerhans cells (LCs) and FcepsilonRIhigh inflammatory dendritic epidermal cells (IDECs). These two DC subtypes are believed to contribute distinctly to the biphasic nature and the outcome of T cell responses in AD. In contrast, plasmacytoid DCs, which play an important role in the defence against viral infections, have been shown to bear the high-affinity receptor for IgE too but are nearly absent from the epidermal skin lesions of AD patients. In light of recent developments, the picture emerges that different IgE-receptor bearing DC subtypes in the blood and skin of AD patients play a pivotal role in the complex network of DCs, which is highlighted in this review.