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 Fcε RII CD23 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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