2003 Volume 24 Issue 6 Pages 291-297
IgG induces both passive and active anaphylaxis but the role of IgG glycosylation in inducing anaphylaxis remains unclear. We sensitized animals to enzymically deglycosylated and native anti-OVA IgG1. Native IgG1 induced passive cutaneous anaphylaxis in Sprague-Dawley rats, showing dye leakage on the rat back, and passive systemic anaphylaxis in ddY mice, showing marked blue coloring of foot pads, significant decreases in rectal temperature and killing all ddY mice within 50 minutes of antigen challenge, while deglycosylated IgG1 completely lost its allergic activity. The abrogation of deglycosylated IgG1 to induce anaphylaxis was not due to the loss of its antigen binding ability because ELISA assay showed that native and deglyeosylated IgG1 had the same ability to bind antigen. Neutralization of lethality in OVA-sensitized mice was found when deglycosylated IgG was intravenously injected 24 hours before challenge with OVA. These results suggest that IgG1-induced anaphylaxis requires IgG1 glycosylation. Deglycosylated IgG may have therapeutic potential for antigen-specific anaphylaxis.
