Enzymically-deglycosylated antibody IgE lost its allergic activity in mouse systemic anaphylaxis, though the IgE kept its antibody activity. IgE antibody obtained from mice treated with a substance extracted from human urine was deglycosylated. This IgE also lost the allergic activity on the systemic anaphylaxis but kept its antibody activity. These findings strongly suggest that glycosylation of IgE has a close relation to the binding of the Fc receptor and that humans have another antiallergic mechanism: in vivo IgE antibody deglycosylation induced by the substance.