Abstract
Allergic reactions arise when people become sensitized to otherwise harmless environmental antigens. In this issue, Shade et al. reveal that the immunoglobulin e (IgE) antibodies that mediate these reactions have a key vulnerability. They report that the ability of IgE to trigger an allergic reaction through its interaction with mast cells is dependent on a single site of antibody glycosylation. With the in vivo targeting of specific glycoprotein glycans emerging as a viable strategy for modulating endogenous glycoprotein function, these findings are of significant interest.
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