Author:
Cruse Glenn,Yin Yuzhi,Fukuyama Tomoki,Desai Avanti,Arthur Greer K.,Bäumer Wolfgang,Beaven Michael A.,Metcalfe Dean D.
Abstract
Allergic diseases are driven by activation of mast cells and release of mediators in response to IgE-directed antigens. However, there are no drugs currently available that can specifically down-regulate mast cell function in vivo when chronically administered. Here, we describe an innovative approach for targeting mast cells in vitro and in vivo using antisense oligonucleotide-mediated exon skipping of the β-subunit of the high-affinity IgE receptor (FcεRIβ) to eliminate surface high-affinity IgE receptor (FcεRI) expression and function, rendering mast cells unresponsive to IgE-mediated activation. As FcεRIβ expression is restricted to mast cells and basophils, this approach would selectively target these cell types. Given the success of exon skipping in clinical trials to treat genetic diseases such as Duchenne muscular dystrophy, we propose that exon skipping of FcεRIβ is a potential approach for mast cell-specific treatment of allergic diseases.
Funder
Division of Intramural Research, National Institute of Allergy and Infectious Diseases
HHS | NIH | National Heart, Lung, and Blood Institute
Publisher
Proceedings of the National Academy of Sciences
Cited by
22 articles.
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