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IgE-Dependent and Independent Effector Mechanisms in Human and Murine Anaphylaxis

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Anaphylaxis and Hypersensitivity Reactions

Abstract

Anaphylaxis is shock mediated by cells of the innate immune system. Studies in murine models demonstrate at least three pathways: (1) antigen cross-linking of IgE bound to Fcε(epsilon)RI leads to mast cell degranulation with release of histamine and PAF; (2) antigen-IgG complexes cross-link Fcγ(gamma)RIII on mast cells and basophils with secretion of PAF; and (3) complement activation leads to production of C3a and C5a, which activate mast cells, basophils, and macrophages. C3a and C5a appear unable to induce shock by themselves in the murine models, but can exacerbate anaphylaxis induced by the other mechanisms. Anaphylaxis can also be exacerbated by IL-4 and IL-13, which increase effector cell responsiveness to vasoactive mediators, and by β(beta)-adrenergic receptor antagonists, which decrease ability to compensate for vascular leak and decreased intravascular volume. IgG-dependent anaphylaxis requires much higher concentrations of antibody and antigen than IgE-mediated anaphylaxis; consequently, IgG antibodies can block the development of anaphylaxis when antigen quantity is low by binding to antigen before it can cross-link mast cell-associated IgE, but can mediate anaphylaxis when antigen quantity is high. Inhibitory receptors, such as Fcγ(gamma)RIIb, can suppress mast cell activation and anaphylaxis, but this effect is less important in our models than IgG neutralization of antigen. Although human IgE anaphylaxis is well established, the existence of IgG-mediated human anaphylaxis is unproven. However, we believe that studies of human anaphylaxis associated with infusion of large quantities of foreign proteins, such as chimeric monoclonal antibodies, make it likely that this type of human anaphylaxis can occur. Elucidation of these mechanisms suggests prophylactic and therapeutic approaches and goals for future anaphylaxis research.

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Abbreviations

Ab:

Antibody

Ag:

Antigen

Fcε(epsilon)RI:

High-affinity receptor for IgE

Fcγ(gamma)RIII:

Low-affinity receptor 3 for IgG

IgE:

Immunoglobulin E

IgG:

Immunoglobulin G

mAb:

Monoclonal antibody

PAF:

Platelet-activating factor

PCA:

Passive cutaneous anaphylaxis

R:

Receptor

TNP:

Trinitrophenyl

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Acknowledgments

This work was supported by a merit award from the US Department of Veterans Affairs and NIH grant R21AI079947. I thank my colleagues Marat Khodoun, Suzanne Morris, and Richard Strait, who performed much of the work described in this review.

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  1. University of Cincinnati College of Medicine, Cincinnati, OH, USA

    Fred D. Finkelman

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  1. Fred D. Finkelman
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Correspondence to Fred D. Finkelman .

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  1. Harvard Medical School, Ambulatory Center, Brigham and Women’s Hospital, Boyleston Street, Route 9 850, Chestnut Hill, 02467, Massachusetts, USA

    Mariana C. Castells

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Finkelman, F.D. (2011). IgE-Dependent and Independent Effector Mechanisms in Human and Murine Anaphylaxis. In: Castells, M. (eds) Anaphylaxis and Hypersensitivity Reactions. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60327-951-2_8

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  • DOI: https://doi.org/10.1007/978-1-60327-951-2_8

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