Abstract

IgE antibodies play a crucial role in allergic reactions, including systemic anaphylaxis, by binding to the high-affinity IgE Fc receptor FcεRI on mast cells and basophils and thereby inducing the release of inflammatory mediators.1,2,E1-E3 In contrast, allergen-specific IgG antibodies, induced also in response to allergen-specific immunotherapies, can suppress IgE-mediated anaphylaxis via allergen masking and particularly crosslinking FcεRI with the IgG inhibitory receptor FcγRIIB.1-3,E1,E4-E6 However, when allergen levels are high, for example, medical drugs, IgG antibodies also have the potential to mediate anaphylaxis by crosslinking classical activating FcγRs, which is also controlled by FcγRIIB, on different innate immune cell types.

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