Systemic anaphylaxis in the mouse can be mediated largely through IgG1 and Fc gammaRIII. Assessment of the cardiopulmonary changes, mast cell degranulation, and death associated with active or IgE- or IgG1-dependent passive anaphylaxis. (original) (raw)

Research Article Free access | 10.1172/JCI119255

D Dombrowicz, T R Martin, J V Ravetch, J P Kinet, and S J Galli

Department of Pathology, Beth Israel Deaconess Medical Center-East and Harvard Medical School, Boston, Massachusetts 02215, USA.

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Department of Pathology, Beth Israel Deaconess Medical Center-East and Harvard Medical School, Boston, Massachusetts 02215, USA.

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Department of Pathology, Beth Israel Deaconess Medical Center-East and Harvard Medical School, Boston, Massachusetts 02215, USA.

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Department of Pathology, Beth Israel Deaconess Medical Center-East and Harvard Medical School, Boston, Massachusetts 02215, USA.

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Department of Pathology, Beth Israel Deaconess Medical Center-East and Harvard Medical School, Boston, Massachusetts 02215, USA.

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Department of Pathology, Beth Israel Deaconess Medical Center-East and Harvard Medical School, Boston, Massachusetts 02215, USA.

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Published March 1, 1997 -More info

Published March 1, 1997 -Version history

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Abstract

We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE- or IgG1-dependent anaphylaxis, in mice lacking either the Fc epsilonRI alpha chain or the FcR gamma chain common to Fc epsilonRI and Fc gammaRI/III, or in mice lacking mast cells (KitW/ KitW-v 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 Fc epsilonRI alpha chain -/- mice than in the corresponding normal mice. Finally, while both KitW/KitW-v 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 Fc epsilonRI 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 gammaRIII.

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