Anti-IgE Agents

There is little debate over the essential role of IgE in allergic reactions. During an allergic response, CD4 + T lymphocytes of the Th2 phenotype stimulate allergen-specific B cells to produce IgE molecules via the release of IL-4/IL-13. The receptors for IgE are found on a multitude of different cells and two different types have been identified: the high-affinity receptor (FcεRI) on mast cells, basophils, and antigen-presenting cells, and the low-affinity receptor (FcεRII or CD23) on B lymphocytes, monocytes/macrophages, eosinophils, dendritic cells, and epithelial cells. After interaction with allergens, IgE-armed cells release a number of inflammatory mediators and enhance and redirect antigen presentation. This cascade of events seems to have a crucial role in the generation and persistence of symptoms in allergic diseases. The development of drugs that interfere with IgE production and function may therefore represent a more specific approach to treat these pathological conditions [1, 2].