Abstract
The propensity to develop an exaggerated antibody response to inhaled antigens operated by immunoglobulin E (IgE), which is defined as atopy, plays a central role in the pathobiology of allergic asthma [1]. The pleiotropic effects of IgE are mediated by activation of specific IgE receptors expressed by both immune-inflammatory and airway structural cells [2–4]. IgE were identified in 1967 by Ishizaka and Ishizaka, and since then these antibodies have been considered as suitable molecular targets for the development of anti-allergy therapies [5, 6]. However, it took almost 40 years to translate this key immunological discovery into the approval of the anti-IgE antibody omalizumab for the treatment of severe allergic asthma [7]. Indeed, omalizumab has been the first and for a long time the only biologic drug available in clinical practice for add-on therapy of uncontrolled asthma [8].
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Pelaia, G., Vatrella, A., Maselli, R. (2017). Anti-IgE Therapy. In: Asthma: Targeted Biological Therapies. Springer, Cham. https://doi.org/10.1007/978-3-319-46007-9_4
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