Publications

Publications, Books, Book Chapters and Reviews by Prof. Marcus Maurer, MD

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The potential pharmacologic mechanisms of omalizumab in patients with chronic spontaneous urticaria

Filename 92. Chang et al., Potential pharm. mech. Omalizumab CSU, JACI 2015.pdf
Filesize 582 KB
Version r.092
Date added June 25, 2020
Downloaded 0 times
Category Reviews
Tags activation/release threshold, autoanti- bodies, Chronic Urticaria, FcεRI, IgE, IgE–FcεRI–mast cell axis, mast cells, omalizumab
Authors Chang, T. S., Chen, C., Lin, C.-J., Metz, M., Church, M. K., and Maurer, M.
Citation Chang, T. S., Chen, C., Lin, C.-J., Metz, M., Church, M. K., and Maurer, M.: The potential pharmacologic mechanisms of omalizumab in patients with chronic spontaneous urticaria. J. Allergy Clin. Immunol. 2015: 135; 337-342.
Corresponding authors Church, M. K.
DocNum r.92
DocType PDF
Edition; Page 135; 337-342
IF 12.48
Publisher J. Allergy Clin. Immunol.
ReleaseDate 2015

In patients given a diagnosis of chronic spontaneous urticaria (CSU), there are no obvious external triggers, and the factors that initiate the clinical symptoms of wheal, flare, and itch arise from within the patient. Most patients with CSU have an autoimmune cause: some patients produce IgE autoantibodies against autoantigens, such as thyroperoxidase or double- stranded DNA, whereas other patients make IgG autoantibodies against FcεRI, IgE, or both, which might chronically activate mast cells and basophils. In the remainder of patients with CSU, the nature of the abnormalities has not yet been identified. Accumulating evidence has shown that IgE, by binding to FcεRI on mast cells without FcεRI cross-linking, can promote the proliferation and survival of mast cells and thus maintain and expand the pool of mast cells. IgE and FcεRI engagement can also decrease the release threshold of mast cells and increase their sensitivity to various stimuli through either FcεRI or other receptors for the degranulation process. Furthermore, IgE- FcεRI engagement potentiates the ability of mast cells to store and synthesize de novo inflammatory mediators and cytokines. Administration of omalizumab, by virtue of its ability to deplete IgE, attenuates the multiple effects of IgE to maintain and enhance mast cell activities and hence reduces the ability of mast cells to manifest inflammatory mechanisms in patients with CSU. (J Allergy Clin Immunol 2015;135:337-42.)

(Last update: 08.2021)

Number of publications (original work and reviews) in peer-reviewed journals: 636
Number of original publications in peer-reviewed journals: 462
Number of reviews in peer-reviewed journals: 174
Cumulative IF of publications (original work & reviews) in peer-reviewed journals: 3834,12
Cumulative IF for original publications in peer-reviewed journals: 3043,14
Cumulative IF for reviews in peer-reviewed journals: 790,98
Citations, Hirsch index: (view on Web of Science) 26429