Cell
Volume 75, Issue 5, 3 December 1993, Pages 969-976
Journal home page for Cell

Article
Abolition of anaphylaxis by targeted disruption of the high affinity immunoglobulin E receptor α chain gene

https://doi.org/10.1016/0092-8674(93)90540-7Get rights and content

Abstract

Mast cells and basophils, which are activated by immunoglobulin E (IgE) and allergen, play a prominent role in anaphylaxis. However, they express at least three types of IgE receptor, including the high affinity IgE receptor (FcεRI). The relative contribution of these IgE receptors, and possibly other receptors such as FcεRIICD23 and Mac-2, to the genesis of in vivo anaphylaxis is still unclear. To address this question, we have generated FcεRI-deficient mice. These mice appear normal and express a normal number of mast cells, but they are resistant to cutaneous and systemic anaphylaxis. These data demonstrate that FcεRI is necessary for the initiation of IgE-dependent anaphylactic reactions. Therefore, interfering with its function should be an effective means of treating allergy, regardless of the allergen specificity.

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