Owen, Charles (2007) Immunoglobulin E: role in asthma and allergic disease: lessons from the clinic. Pharmacology & Therapeutics, 113 (1). pp. 121-133. ISSN 0163-7258

Abstract

The role of immunoglobulin E (IgE) in allergic asthmatic disease is well established. Allergen-specific IgE binds to its cognate receptors, thus triggering a series of cellular events. These events include presentation of antigen by dendritic cells and the degranulation of mast cells and basophils to release numerous factors that play an integral part in potentiating the disease symptoms. Studies in the mouse indicate that a reduction in IgE levels could lead to significant attenuation of the allergic inflammatory response associated with diseases such as asthma, making IgE a target for the development of new therapeutic agents. Omalizumab (Xolair), a recombinant humanised monoclonal anti-IgE antibody that blocks the interaction of IgE with its receptors, is the first anti-IgE agent to undergo clinical development. Several clinical studies have been performed in adults and children with moderate-to-severe allergic asthma to evaluate the efficacy and safety of this agent, but which have also enabled an insight into the role of IgE in human disease. IgE plays a significant role in a number of allergic conditions including allergic rhinitis and allergies to various substances. Recent data suggests that local IgE production may occur in mucosal tissues and that locally significant concentrations of IgE, not reflected by serum IgE concentrations, indicate that it may play a role in non-atopic as well as atopic disease.

Item Type:	Article
Related URLs:	http://www.ncbi.nlm.nih.gov/sites/entrez... doi:10.1016/j.pharmthera.2006.07.003
Additional Information:	author can archive post-print (ie final draft post-refereeing); Publisher's version/PDF cannot be used
Keywords:	Asthma; Immunoglobulin E; Omalizumab; Allergy; Atopy; Anti-IgE
Related URLs:	http://www.ncbi.nlm.nih.gov/sites/entrez... doi:10.1016/j.pharmthera.2006.07.003
Date Deposited:	14 Dec 2009 13:57
Last Modified:	14 Dec 2009 13:57
URI:	https://oak.novartis.com/id/eprint/590