Systemic Anaphylaxis in the Mouse Can Be Mediated Largely through IgG1 and Fc gamma RIII: Assessment of the Cardiopulmonary Changes, Mast Cell Degranulation, and Death Associated with Active or IgE- or IgG1-dependent Passive Anaphylaxis

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We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE-or IgG1-dependent anaphylaxis, in mice lacking either the Fcepsilon RI alpha chain or the FcR gamma chain common to Fcepsilon RI and Fc gamma RI/III, or in mice lacking mast cells (KitW/KitW-nu mice), and compared the responses to those in the corresponding wild-type mice. We found that the FcR gamma chain is required for the death, as well as for most of the pathophysiological changes, associated with active anaphylaxis or IgE- or IgG1-dependent passive anaphylaxis. Moreover, some of the physiological changes associated with either active, or IgG1-dependent passive, anaphylactic responses were significantly greater in Fcepsilon RI alpha chain -/- mice than in the corresponding normal mice. Finally, while both KitW/KitW-nu and congenic +/+ mice exhibited fatal active anaphylaxis, mast cell-deficient mice exhibited weaker physiological responses than the corresponding wild-type mice in both active and IgG1-dependent passive systemic anaphylaxis. Our findings strongly suggest that while IgE antibodies and Fcepsilon 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 IgG1 antibodies and Fc gamma RIII. (J. Clin. Invest. 1997. 99:901-914.)

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