Abstract
RATIONALE: An IgE-mediated allergic response requires allergen-specific B-cell differentiation into IgE-producing plasma cells. B-cell activation is suppressed by BCR coengagement with inhibitory receptor FcγRIIb; therefore, we reasoned that an anti-IgE IgG engineered for high Fc domain affinity to FcγRIIb would coengage IgE-BCR and FcγRIIb, specifically deactivating IgE+ B cells. We describe XmAb6728 as a novel therapeutic based on omalizumab (Xolair) that binds the same epitope of soluble IgE but also uniquely suppresses IgE+ B cells.
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