SYSTEMIC-ANAPHYLAXIS IN THE MOUSE CAN BE MEDIATED LARGELY THROUGH IGG, AND FC-GAMMA-RIII - ASSESSMENT OF THE CARDIOPULMONARY CHANGES, MAST-CELL DEGRANULATION, AND DEATH ASSOCIATED WITH ACTIVE OR IGE-DEPENDENT OR IGG(1)-DEPENDENT PASSIVE ANAPHYLAXIS

We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE - or IgG(1)-dependent anaphylaxis, in mice lacking either the Fc(epsil on)RI alpha chain or the FcR gamma chain common to Fc(epsilon)RI and F c gamma 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 mic e. We found that the FcR gamma chain is required for the death, as wel l as for most of the pathophysiological changes, associated with activ e anaphylaxis or IgE- or IgG(1)-dependent passive anaphylaxis. Moreove r, some of the physiological changes associated with either active, or IgG(1)-dependent passive, anaphylactic responses were significantly g reater in Fc(epsilon)RI alpha chain -/- mice than in the corresponding normal mice. Finally, while both Kit(W)/Kit(W-v) and congenic +/+ mic e exhibited fatal active anaphylaxis, mast cell-deficient mice exhibit ed weaker physiological responses than the corresponding wild-type mic e in both active and IgG(1)-dependent passive systemic anaphylaxis. Ou r findings strongly suggest that while IgE antibodies and Fc(epsilon)R I may influence the intensity and/or kinetics of some of the pathophys iological changes associated with active anaphylaxis in the mouse, the mortality associated with this response can be mediated largely by Ig G(1) antibodies and Fc gamma-RIII.