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.

Miyajima, Ichiro; Dombrowicz, David; Martin, Thomas R.; Ravetch, Jeffrey V.; Kinét, Jean Pierre; Galli, Stephen J.

doi:10.1172/jci119255

Cited by 335 publications

(264 citation statements)

References 38 publications

Supporting

Mentioning

236

Contrasting

Unclassified

Order By: Relevance

“…We noted that the skin from Fc⑀RI␣ Ϫ/Ϫ and wild-type mice have comparable numbers of mast cells when stained with toluidine blue, consistent with previous reports (36,37). The number of mast cells per 100-mm 2 dermis was 7.9 Ϯ 1.6 for wild-type mice and 9.2 Ϯ 2.1 for Fc⑀RI␣ Ϫ/Ϫ mice.…”

Section: Generation Of Fc⑀ri␣ ϫ/ϫ Micesupporting

confidence: 91%

IgE-Dependent Mast Cell Activation Potentiates Airway Responses in Murine Asthma Models

Mayr

Zuberi

Zhang

et al. 2002

The Journal of Immunology

View full text Add to dashboard Cite

We have studied murine models of asthma using FcεRIα-chain-deficient (FcεRIα−/−) mice to investigate the role of IgE-dependent mast cell activation in these models. When mice were either 1) immunized once with OVA in alum i.p. and then challenged with OVA intranasally, or 2) repeatedly immunized with OVA in the absence of adjuvant and subsequently challenged with nebulized OVA, FcεRα−/− mice had significantly fewer eosinophils and lower IL-4 levels in their bronchoalveolar lavage fluid compared with wild-type mice. When mice were given anti-IL-5 antibody before OVA challenge in protocol 1, eosinophilic infiltration into the airways was significantly suppressed in both genotypes, but only FcεRIα−/− mice showed significantly reduced airway hyperresponsiveness (AHR). In addition, when mice immunized and challenged with OVA also received a late OVA provocation at a higher concentration and were then exposed to methacholine, only wild-type mice developed a substantial increase in AHR. Since FcεRI is expressed mainly on mast cells in mouse airways, we conclude that IgE-dependent activation of this cell type plays an important role in the development of allergic airway inflammation and AHR in mice. The models used may be of value for testing inhibitors of IgE or mast cells for development of therapeutic agents for human asthma.

show abstract

Section: Generation Of Fc⑀ri␣ ϫ/ϫ Micesupporting

confidence: 91%

IgE-Dependent Mast Cell Activation Potentiates Airway Responses in Murine Asthma Models

Mayr

Zuberi

Zhang

et al. 2002

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…3C), consistent with a recent study demonstrating that human mast cells express this receptor (8). To test whether WSX-1 directly regulates mast cell activity, an in vivo model of mast cell-dependent passive cutaneous anaphylaxis was used (29,30). In these studies, WT and WSX-1 Ϫ/Ϫ mice were primed with intradermal injections of anti-DNP-IgE.…”

Section: Wsx-1 Is a Negative Regulator Of Mast Cell Responsessupporting

confidence: 58%

The IL-27 Receptor (WSX-1) Is an Inhibitor of Innate and Adaptive Elements of Type 2 Immunity

Artis¹,

Villarino²,

Silverman

et al. 2004

The Journal of Immunology

223

210

View full text Add to dashboard Cite

Although previous studies have investigated the role of IL-27/WSX-1 interactions in the regulation of Th1 responses, little is known about their role in regulating Th2-type responses. Studies presented in this work identify a direct role for IL-27/WSX-1 interactions in the negative regulation of type 2 responses independent of effects on type 1 cytokines. WSX-1−/− mice infected with the gastrointestinal helminth Trichuris muris displayed accelerated expulsion of parasites and the development of exaggerated goblet cell hyperplasia and mastocytosis in the gut due to increased production of Th2 cytokines. Enhanced mast cell activity in the absence of WSX-1 was consistent with the ability of wild-type mast cells to express this receptor. In addition, IL-27 directly suppressed CD4+ T cell proliferation and Th2 cytokine production. Together, these studies identify a novel role for IL-27/WSX-1 in limiting innate and adaptive components of type 2 immunity at mucosal sites.

show abstract

“…24 h later with TNP-OVA. The severity of the anaphylactic shock was assessed by change in rectal temperature (4,44). Histamine and PAF antagonists were used in some experiments to suppress anaphylaxis (4).…”

Section: Methodsmentioning

confidence: 99%

Identification of markers that distinguish IgE- from IgG-mediated anaphylaxis

Khodoun

Strait

Armstrong

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

124

107

View full text Add to dashboard Cite

IgG-mediated anaphylaxis occurs in mice and may contribute to human reactions to infused drugs. To distinguish IgE- from putative IgG-mediated human anaphylaxis, we developed blood markers for murine anaphylaxis and evaluated their human relevance. Both IgG- and IgE-mediated anaphylaxis were characterized by decreased basophil and monocyte percentages and an increased neutrophil percentage in mouse blood. IgE- but not IgG-mediated murine anaphylaxis was accompanied by large increases in IL-4 secretion, plasma soluble IL-4 receptor-α (IL-4Rα) concentration, and T-cell membrane IL-4Rα expression. T-cell IL-4Rα expression also increased when mice that express human Fcε receptor Iα were sensitized with IgG-depleted serum from a peanut-allergic individual and challenged with peanut extract. Increased T-cell IL-4Rα expression is likely to also be a marker for human IgE-mediated anaphylaxis, because IgE-activated human basophils secrete IL-4, and IL-4 increases human T-cell IL-4Rα expression in vitro. Murine IgG- but not IgE-mediated anaphylaxis was characterized by decreased neutrophil Fcγ receptor III (FcγRIII) expression that was observed even when the antigen dose was insufficient to induce shock. Human neutrophils cultured with IgG immune complexes also lost FcγRIII. These observations suggest that decreased blood neutrophil FcγRIII expression without increased IL-4Rα expression can be used to determine whether and when IgG-mediated anaphylaxis occurs in man.

show abstract

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.

Abstract: We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE-or IgG 1 -dependent anaphylaxis, in mice lacking either the Fc ⑀ RI ␣ chain or the FcR ␥ chain common to

Cited by 335 publications

References 38 publications

IgE-Dependent Mast Cell Activation Potentiates Airway Responses in Murine Asthma Models

IgE-Dependent Mast Cell Activation Potentiates Airway Responses in Murine Asthma Models

The IL-27 Receptor (WSX-1) Is an Inhibitor of Innate and Adaptive Elements of Type 2 Immunity

Identification of markers that distinguish IgE- from IgG-mediated anaphylaxis

Contact Info

Product

Resources

About