The high-affinity receptor for immunoglobulin E (IgE), FcεRI, plays a central role in the initiation and control of atopic allergic inflammation. On mast cells and basophils, the function of the receptor is well known and constitutes cellular degranulation and the release of various mediators. FcεRI on antigen-presenting cells (APCs), however, does not lead to degranulation of preformed granula, but has different functions: signal transduction pathways like the activation of NF-κB are initiated to induce inflammatory cytokine gene expression. In addition, FcεRI on APCs acts as an allergen-focusing structure and can efficiently amplify allergen presentation in an IgE-dependent manner. Recently, we and others have gained new insight into the regulation and function of FcεRI on APCs, which has shed new light on the modulating effects of the immune system in atopic inflammation.