IgE-mediated food allergy is a growing problem with no curative therapy1. Oral immunotherapy (OIT) has shown promise, but its utility is limited by reactions during treatment and a lack of sustained protection following therapy. IgE antibodies trigger hypersensitivity reactions to foods. Their effects, mediated by FcεRI on mast cells and basophils, can be countered by IgG antibodies of shared specificity signaling via the inhibitory Fc receptor, FcγRIIb2. OIT induces only modest reductions in specific IgE antibodies but stimulates dramatic increases in inhibitory IgG3, 4.
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