The potential pharmacologic mechanisms of omalizumab in patients with chronic spontaneous urticaria Tse Wen Chang, PhD, Christina Chen, BS, Chien-Jen.

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Presentation transcript:

The potential pharmacologic mechanisms of omalizumab in patients with chronic spontaneous urticaria Tse Wen Chang, PhD, Christina Chen, BS, Chien-Jen Lin, PhD, Martin Metz, MD, Martin K. Church, PhD, DSc, Marcus Maurer, MD Journal of Allergy and Clinical Immunology Volume 135, Issue 2, Pages 337-342.e2 (February 2015) DOI: 10.1016/j.jaci.2014.04.036 Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 The inflammatory manifestation of mast cells in affected skin is the final common pathway in various types of urticaria. For the inducible subtypes, there are identifiable external triggers. For physical urticaria, the internal pathologic factors that transduce external triggers to mast cell activation have not been identified. For the spontaneous type, the primary causative factors that cause the urticarial manifestation arise internally. In one large subtype the patients have an autoimmune cause. For the remaining cases of the spontaneous type, the internal abnormalities have not been identified. Journal of Allergy and Clinical Immunology 2015 135, 337-342.e2DOI: (10.1016/j.jaci.2014.04.036) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 The potentiating effects of IgE on mast cell activity. Binding of monomeric IgE to FcεRI, without IgE cross-linking, potentiates the activities of mast cells in the absence of degranulation. Compared with mast cells without IgE engagement, the IgE-engaged mast cells become more sensitive as the thresholds for activation and degranulation (release thresholds) by various factors through their receptors are decreased. The mast cells also become more potent because they store more mediators and can synthesize more mediators on degranulation. The mast cells also synthesize an array of factors and cytokines, which promote both differentiation of progenitors to become mast cells and survival of mast cells, thus augmenting the pool of mast cells. In subjects with anti-IgE autoantibodies, IgE autoantibodies, or both, the anti-IgE autoantibodies and presence of cross-reactive self-antigens can cause subthreshold levels of IgE cross-linking and FcεRI aggregation and augment the IgE-potentiating effect of mast cells. Journal of Allergy and Clinical Immunology 2015 135, 337-342.e2DOI: (10.1016/j.jaci.2014.04.036) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions