OBJECTIVE The manifestation of atopic eczema/dermatitis syndrome is believed to result from a complex interrelationship of environmental factors, pharmacological abnormalities, skin barrier defects, and immunological phenomena. Although we are only beginning to understand the molecular basis of this disease, much progress has been made in defining key events leading to the manifestation of allergic inflammation. Here, we review recent findings that underscore the importance of dendritic cells as being central to shape these proinflammatory responses. RESULTS Evidence for a differential regulation of the high affinity receptor for IgE, Fc epsilon RI, on the surface of atopic dendritic cells compared with non-atopic dendritic cells became apparent. In atopic donors, in contrast to non-atopic donors, the intracellular expression of the gamma-chains of Fc epsilon RI is sufficient, thus leading to the assembly with the alpha-chain and surface expression of the receptor. This finding is of considerable interest for an understanding of the pathophysiology of IgE-mediated dendritic cell functions in atopic eczema/dermatitis syndrome. In addition, it has been shown that keratinocytes from the epidermal skin of individuals with atopic eczema/dermatitis syndrome express human thymic stromal lymphopoietin, which activates dendritic cells to attract T helper type 2 cells into the skin. Furthermore, these activated dendritic cells prime naïve T cells into T helper type 2 cells. CONCLUSIONS The past few years have seen a remarkable process of refocusing in atopy. Dendritic cells in particular have been at the centre of this process. It has become unequivocally clear that these cells have the power of shaping the allergic response.