• Konstantinos Samitas, Vasiliki Delimpoura, Eleftherios Zervas, and Mina Gaga.
• 7th Respiratory Dept and Asthma Centre, Athens Chest Hospital "Sotiria", Athens, Greece Cellular Immunology Laboratory, Division of Cell Biology, Centre for Basic Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.
• Eur Respir Rev. 2015 Dec 1; 24 (138): 594-601.

AbstractAsthma is a disorder of the airways involving various inflammatory cells and mediators and characterised by bronchial hyperresponsiveness, chronic inflammation and structural alterations in the airways, also known as remodelling. IgE is an important mediator of allergic reactions and has a central role in allergic asthma pathophysiology, as it is implicated in both the early and late phase allergic response. Moreover, clinical and mechanistic evidence has lately emerged, implicating IgE in the development of airway remodelling. The use of monoclonal antibodies targeting IgE, such as omalizumab, has proven very effective in improving respiratory symptoms and quality of life, while reducing asthma exacerbations, emergency room visits and the use of systemic corticosteroids in allergic severe asthma. These effects are believed to be mainly mediated by omalizumab's inhibitory effect on the initiation and further propagation of the allergic inflammation cascade. However, there is evidence to suggest that anti-IgE treatment remains effective long after it has been discontinued. In part, these findings could be attributed to the possible ameliorating effects of anti-IgE treatment on airway remodelling. In this review, we discuss recent findings supporting the notion that anti-IgE treatment modulates the complex immune responses that manifest clinically as asthma and ameliorates airway remodelling changes often observed in allergic severe asthma phenotypes. Copyright ©ERS 2015.

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