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Mouse and human neutrophils induce anaphylaxis
Friederike Jönsson, … , Marc Daëron, Pierre Bruhns
Friederike Jönsson, … , Marc Daëron, Pierre Bruhns
Published March 23, 2011
Citation Information: J Clin Invest. 2011;121(4):1484-1496. https://doi.org/10.1172/JCI45232.
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Research Article Article has an altmetric score of 34

Mouse and human neutrophils induce anaphylaxis

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Abstract

Anaphylaxis is a life-threatening hyperacute immediate hypersensitivity reaction. Classically, it depends on IgE, FcεRI, mast cells, and histamine. However, anaphylaxis can also be induced by IgG antibodies, and an IgG1-induced passive type of systemic anaphylaxis has been reported to depend on basophils. In addition, it was found that neither mast cells nor basophils were required in mouse models of active systemic anaphylaxis. Therefore, we investigated what antibodies, receptors, and cells are involved in active systemic anaphylaxis in mice. We found that IgG antibodies, FcγRIIIA and FcγRIV, platelet-activating factor, neutrophils, and, to a lesser extent, basophils were involved. Neutrophil activation could be monitored in vivo during anaphylaxis. Neutrophil depletion inhibited active, and also passive, systemic anaphylaxis. Importantly, mouse and human neutrophils each restored anaphylaxis in anaphylaxis-resistant mice, demonstrating that neutrophils are sufficient to induce anaphylaxis in mice and suggesting that neutrophils can contribute to anaphylaxis in humans. Our results therefore reveal an unexpected role for IgG, IgG receptors, and neutrophils in anaphylaxis in mice. These molecules and cells could be potential new targets for the development of anaphylaxis therapeutics if the same mechanism is responsible for anaphylaxis in humans.

Authors

Friederike Jönsson, David A. Mancardi, Yoshihiro Kita, Hajime Karasuyama, Bruno Iannascoli, Nico Van Rooijen, Takao Shimizu, Marc Daëron, Pierre Bruhns

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Figure 5

Neutrophils and basophils contribute to active anaphylaxis in WT mice.

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Neutrophils and basophils contribute to active anaphylaxis in WT mice.
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(A) Representative histogram plots of FcγRIIIA expression in WT mice on cell populations identified as in Figure 1D. (B–E) Indicated mice were immunized against BSA and challenged with BSA. Central temperatures and survival rates were monitored. (B) WT mice were injected with gadolinium or vehicle before BSA challenge (n = 4). (C) WT mice were injected with anti-Gr1, anti-CD200R3, anti-Gr1 plus anti-CD200R3 mAbs (n = 4), or isotype controls (n = 5) before BSA challenge. Survival of the isotype-treated group is statistically different from the anti-Gr1 and from the anti-Gr1 plus anti-CD200R3 groups (P < 0.05), but not from the anti-CD200R3 group. (D) Wsh mice were injected with anti-CD200R3 (top: n = 3; bottom: n = 4), anti-Gr1 (top: n = 4), anti-Gr1 plus anti-CD200R3 (top: n = 5; bottom: n = 4) mAbs, or isotype controls (top: n = 4; bottom: n = 3) before BSA challenge. (E) FcγRIIIA–/– mice injected with anti-Gr1 mAbs or isotype control before BSA challenge (n = 5). (B–E) Data are represented as mean ± SEM. (A–E) Data are representative of 2 independent experiments. **P < 0.01. X’s represent 100% mortality in the experimental group.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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