Anti-IgE therapy in allergic disease

Purpose of review Recombinant monoclonal humanized anti-IgE has put forward a fundamentally new concept for the control of allergic disorders. This review will present recent data from clinical studies with anti-IgE in asthma, allergic rhinitis, and food allergy and will examine the place of anti-IgE among current therapeutic options for the treatment of asthma. Recent findings Therapy with anti-IgE depresses circulating free IgE to the limits of detection, inhibits early- and late-phase responses to allergens, suppresses inflammation and improves the control of allergic diseases. In moderate to severe asthma it results in fewer exacerbations and a lower requirement for both corticosteroids and beta-agonists. IgE appears to be an important regulator of high-affinity Fc receptors (FcepsilonRI) and, in the mouse, to enhance mast cell survival and activation. IgE receptors have been found on diverse inflammatory cells. Anti-IgE reduces the expression of FcepsilonRI on inflammatory cells. Current work has documented a marked decrease in tissue eosinophils, lymphocytes, and interleukin-4-positive cells by anti-IgE treatment and has provided insight into the mechanisms underlying improved control of asthma. Summary Clinical studies with anti-IgE have promoted and will continue to advance the understanding of IgE-mediated disease mechanisms. They have documented its efficacy in the treatment of allergic diseases, but much remains to be learned about the most effective clinical strategies and the selection of patients for therapy.