Over the last three decades, a good deal of work has focused on the IgE response due to the implication of these antibodies in allergic diseases. IgE antibodies, mediators of immediate hypersensitivity reactions, bind to specific high or low affinity receptors which are distributed on cell surfaces throughout the organism. Activation of receptors contributes to the different aspects of allergic inflammation. Regulation of the IgE response is complex and involves different factors modulating isotype synthesis, low-affinity receptor FcERII:CD23 and its soluble portion, and the Th1/Th2 balance. Allergic diseases are characterized by a dysregulated IgE response, probably related to an imbalance favoring Th2 leading to exaggerated reaction. The advent of anti-IgE treatments can be seen as a notable progress in the management of atopic diseases. Their contribution will depend on the exact role of the IgE response in inflammatory allergic reactions.