Identification of the low affinity receptor for immunoglobulin E on mouse mast cells and macrophages as Fc gamma RII and Fc gamma RIII.

Takizawa, Fumiyoshi; Adamczewski, Martin; Kinét, Jean-Pierre

doi:10.1084/jem.176.2.469

Cited by 132 publications

(84 citation statements)

References 35 publications

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“…Stimulation of mast cells through Fc␥RIII with oligomeric IgE induced serotonin secretion in vitro (5). This study provided the first evidence that IgE could bind Fc␥RIII and stimulates mast cells via this receptor.…”

Section: Ige-mediated Activation Of Nk Cellsmentioning

confidence: 78%

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IgE-Mediated Activation of NK Cells Through FcγRIII

Arase

Hirano

et al. 2003

The Journal of Immunology

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NK cells express FcγRIII (CD16), which is responsible for IgG-dependent cell cytotoxicity and for production of several cytokines and chemokines. Whereas FcγRIII on NK cells is composed of both FcγRIIIα and FcRγ chains, that on mast cells is distinct from NK cells and made of FcγRIIIα, FcRβ, and FcRγ. Mast cells show degranulation and release several mediators, which cause anaphylactic responses upon cross-linking of FcγRIII as well as FcεRI with aggregated IgE. In this paper, we examined whether IgE activates NK cells through FcγRIII on their cell surface. We found that NK cells produce several cytokines and chemokines related to an allergic reaction upon IgE stimulation. Furthermore, NK cells exhibited cytotoxicity against IgE-coated target cells in an FcγRIII-dependent manner. These effects of IgE through FcγRIII were not observed in NK cells from FcRγ-deficient mice lacking FcγRIII expression. Collectively, these results demonstrate that NK cells can be activated with IgE through FcγRIII and exhibit both cytokine/chemokine production and Ab-dependent cell cytotoxicity. These data imply that not only mast cells but also NK cells may contribute to IgE-mediated allergic responses.

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Section: Ige-mediated Activation Of Nk Cellsmentioning

confidence: 78%

“…It was demonstrated that IgE binds to Fc␥RIII on a mast cell line in vitro and causes degranulation (5). Furthermore, when IgE-mediated anaphylaxis was compared between Fc␥RIII Ϫ/Ϫ and wildtype (wt) 3 mice, the anaphylaxis was more severe in wt mice than in Fc␥RIII Ϫ/Ϫ mice (6).…”

Section: Ige-mediated Activation Of Nk Cellsmentioning

confidence: 99%

IgE-Mediated Activation of NK Cells Through FcγRIII

Arase

Hirano

et al. 2003

The Journal of Immunology

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“…Serum IgG levels are generally much higher than IgE levels. Consequently, although IgE IC can interact with mouse FcγRIIb and FcγRIII, at least in vitro at 4°C (30), the quantity of IgG IC is likely to be considerably higher than the quantity of IgE IC in the same animal. With this in mind, we hypothesized that IgG-but not IgE-mediated anaphylaxis might be accompanied by a change in FcγRIII expression by nucleated blood cells.…”

Section: Resultsmentioning

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

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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.

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“…IgE ICs bound as efficiently as IgG2b ICs to mFcγRIV, less efficiently to mFcγRIIB and mFcγRIIIA, and not detectably to mFcγRI. mFcγRIIB and mFcγRIIIA were previously reported to behave as low-affinity IgE receptors (15). IgE ICs of the 2 allotypes bound comparably to mFcγRIV ( Figure 1C).…”

Section: Mfcγriv But Not Hfcγriii Is a Low-affinity Ige Receptormentioning

confidence: 97%

FcγRIV is a mouse IgE receptor that resembles macrophage FcεRI in humans and promotes IgE-induced lung inflammation

Mancardi¹,

Iannascoli²,

Hoos³

et al. 2008

J. Clin. Invest.

135

144

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FcγRIV is a recently identified mouse activating receptor for IgG2a and IgG2b that is expressed on monocytes, macrophages, and neutrophils; herein it is referred to as mFcγRIV. Although little is known about mFcγRIV, it has been proposed to be the mouse homolog of human FcγRIIIA (hFcγRIIIA) because of high sequence homology. Our work, however, has revealed what we believe to be new properties of mFcγRIV that endow this receptor with a previously unsuspected biological significance; we have shown that it is a low-affinity IgE receptor for all IgE allotypes. Although mFcγRIV functioned as a high-affinity IgG receptor, mFcγRIV-bound monomeric IgGs were readily displaced by IgE immune complexes. Engagement of mFcγRIV by IgE immune complexes induced bronchoalveolar and peritoneal macrophages to secrete cytokines, suggesting that mFcγRIV may be an equivalent of human FcεRI(αγ), which is expressed by macrophages and neutrophils and especially in atopic individuals, rather than an equivalent of hFcγRIIIA, which has no affinity for IgE. Using mice lacking 3 FcγRs and 2 FcεRs and expressing mFcγRIV only, we further demonstrated that mFcγRIV promotes IgE-induced lung inflammation. These data lead us to propose a mouse model of IgE-induced lung inflammation in which cooperation exists between mast cells and mFcγRIV-expressing lung cells. We therefore suggest that a similar cooperation may occur between mast cells and hFcεRI-expressing lung cells in human allergic asthma.

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Identification of the low affinity receptor for immunoglobulin E on mouse mast cells and macrophages as Fc gamma RII and Fc gamma RIII.

Cited by 132 publications

References 35 publications

IgE-Mediated Activation of NK Cells Through FcγRIII

IgE-Mediated Activation of NK Cells Through FcγRIII

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

FcγRIV is a mouse IgE receptor that resembles macrophage FcεRI in humans and promotes IgE-induced lung inflammation

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