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The rationale for treating allergic asthma with anti-IgE

CORRESPONDENCE: E. Hamelmann, Charité Universitaetsmedizin Berlin, Dept of Paediatric Pneumology and Immunology, Augustenburger Platz 1, 13353 Berlin, Germany. Fax: 49 30450559951. E-mail: eckard.hamelmann{at}charite.de

An estimated two-thirds of asthma is allergic and >50% of severe asthma has an allergic component. An increased immunoglobulin (Ig)E production in response to environmental allergens (atopy) is the strongest detectable predisposing factor for the development of asthma, particularly when sensitisation occurs early in life.

IgE binds to high-affinity receptors (FcRI) on effector cells, such as mast cells and basophils. Allergen binds to IgE and initiates an inflammatory cascade resulting in release of pro-inflammatory mediators that contribute to the acute and chronic symptoms of allergic airway diseases. By reducing serum IgE levels and FcRI receptor expression on key cells in the inflammatory cascade, omalizumab blocks the release of inflammatory mediators from mast cells and reduces the infiltration of inflammatory cells, notably eosinophils, into the airway. In patients with allergic asthma, omalizumab inhibits both the early and late asthmatic response and several other markers of inflammation, including the requirement for inhaled or oral corticosteroids.

The anti-inflammatory effects of omalizumab provide proof-of-concept of the key role played by immunoglobulin E in allergic respiratory disease. Omalizumab represents a novel approach to the treatment of asthma, inhibiting the inflammatory cascade before it starts.

KEYWORDS: Airway inflammation, allergic asthma, anti-immunoglobulin E, immune modulation, monoclonal antibody, omalizumab