Systemic Anaphylaxis in the Mouse Can Be Mediated Largely through IgG

We attempted to elicit active anaphylaxis to ovalbumin, or passive IgEor IgG 1 -dependent anaphylaxis, in mice lacking either the Fc e RI a chain or the FcR g chain common to Fc e RI and Fc g RI/III, or in mice lacking mast cells ( Kit W / Kit W-v mice), and compared the responses to those in the corresponding wild-type mice. We found that the FcR g chain is required for the death, as well as for most of the pathophysiological changes, associated with active anaphylaxis or IgEor IgG 1 -dependent passive anaphylaxis. Moreover, some of the physiological changes associated with either active, or IgG 1 -dependent passive, anaphylactic responses were significantly greater in Fc e RI a chain 2 / 2 mice than in the corresponding normal mice. Finally, while both Kit W /Kit W-v and congenic 1 / 1 mice exhibited fatal active anaphylaxis, mast cell–deficient mice exhibited weaker physiological responses than the corresponding wild-type mice in both active and IgG 1 -dependent passive systemic anaphylaxis. Our findings strongly suggest that while IgE antibodies and Fc e RI may influence the intensity and/or kinetics of some of the pathophysiological changes associated with active anaphylaxis in the mouse, the mortality associated with this response can be mediated largely by IgG 1 antibodies and Fc g RIII. ( J. Clin. Invest. 1997. 99:901–914.)