Regulation of allergy by Fc receptors

Bruhns, Pierre; Frémont, S.; Daëron, Marc

doi:10.1016/j.coi.2005.09.012

Cited by 92 publications

(68 citation statements)

References 51 publications

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“…1). Upon cross-linking of the FcεRI-IgE complex on the mast cell surface with the FcgRIIB-IgG complex by the same multivalent ligand, FcgRIIB ITIM phosphorylation by FcεRI-associated kinases can directly suppress FcεRI signaling and mast cell activation (43,44). In the mouse model of Fel d1-specific IT, both mechanisms have been postulated to contribute to the suppression of the immediate phase of the allergic response (20).…”

Section: Discussionmentioning

confidence: 99%

Suppression of Th2-Driven Airway Inflammation by Allergen Immunotherapy Is Independent of B Cell and Ig Responses in Mice

Shirinbak

Taher

Maazi

et al. 2010

The Journal of Immunology

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Allergen-specific immunotherapy (IT) uniquely renders long-term relief from allergic symptoms and is associated with elevated serum levels of allergen-specific IgG and IgA. The allergen-specific IgG response induced by IT treatment was shown to be critical for suppression of the immediate phase of the allergic response in mice, and this suppression was partially dependent on signaling through FcγRIIB. To investigate the relevance of the allergen-specific IgG responses for suppression of the Th2-driven late-phase allergic response, we performed IT in a mouse model of allergic asthma in the absence of FcγRIIB or FcγRI/FcγRIII signaling. We found that suppression of Th2 cell activity, allergic inflammation, and allergen-specific IgE responses is independent of FcγRIIB and FcγRI/FcγRIII signaling. Moreover, we show that the IT-induced allergen-specific systemic IgG or IgA responses and B cell function are dispensable for suppression of the late-phase allergic response by IT treatment. Finally, we found that the secretory mucosal IgA response also is not required for suppression of the Th2-driven allergic inflammation by IT. These data are in contrast to the suppression of the immediate phase of the allergic response, which is critically dependent on the induced allergen-specific serum IgG response. Hence, IT-induced suppression of the immediate and late phases of the allergic response is governed by divergent and independent mechanisms. Our data show that the IT-induced suppression of the Th2 cell-dependent late-phase allergic response is independent of the allergen-specific IgG and IgA responses that are associated with IT treatment.

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Section: Discussionmentioning

confidence: 99%

Suppression of Th2-Driven Airway Inflammation by Allergen Immunotherapy Is Independent of B Cell and Ig Responses in Mice

Shirinbak

Taher

Maazi

et al. 2010

The Journal of Immunology

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“…It has also been reported that SPE-7 activates mast cells in the absence of Ag (28,30), but that monovalent hapten abolishes these properties (31), suggesting that SPE-7 auto-aggregates due to a low affinity for its own structure and/or recognizes other cell surface components (32) (reviewed in ref. 33). Altogether, these data obtained by others strongly support our data that SPE-7 contains high-molecular weight aggregates, induces activation in the absence of Ag, and binds other molecules than DNP and IgE-binding molecules, including mFcγRI.…”

Section: Human Fcεri(αγ) Is a Functional Equivalent Of Mouse Fcγrivmentioning

confidence: 99%

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.

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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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“…The significance of FcgRIIB-mediated negative regulation of immune responses has been established largely through the use of mice deficient in or having enhanced expression of this receptor (25). FcgRIIB deficiency is associated with increased inflammation, allergy, and development of chronic autoimmunity (26,29,30). Moreover, these knockout mice were described to display impaired mucosal tolerance after nasal administration of Ag (OVA), resulting in reduced suppression of eosinophilia and IgE production in murine allergic rhinitis and delayed-type hypersensitivity (DTH) reactions, which was assumed to reflect the lack of FcgRIIB expression on DCs (30,31).…”

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confidence: 99%

Important Role for FcγRIIB on B Lymphocytes for Mucosal Antigen-Induced Tolerance and Foxp3+ Regulatory T Cells

Sun

Zou

Smith³

et al. 2013

The Journal of Immunology

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FcγRIIB, the only FcγR expressed on B cells, is important in the maintenance of immunological tolerance to self-Ags. In this study, we investigated the role of FcγRIIB in Ag-specific CD4 T cell tolerance induced by mucosally administered Ag (OVA) coupled to cholera toxin B subunit (Ag/CTB) or given alone. We found that sublingual administration of Ag/CTB conjugate or intragastric administration of a >100-fold higher dose of Ag alone efficiently suppressed parenteral immunization–induced Ag-specific T cell proliferation and delayed-type hypersensitivity responses in FcγRIIB-expressing wild-type (WT), but not FcγRIIB−/−, mice. Such mucosally induced tolerance (oral tolerance) associated with induction of Ag-specific Foxp3+ regulatory T cells was restored in FcγRIIB−/− mice by adoptive transfer of either WT B cells or WT dendritic cells before the mucosal Ag/CTB treatment; it was even more pronounced in μMT mice that received FcγRIIB-overexpressing B cells before treatment. Furthermore, cell transfer in either WT or μMT mice of WT but not FcγRIIB−/− B cells pretreated for 1 h in vitro with Ag/CTB conjugate induced Ag-specific immunological tolerance, which was further enhanced by adoptive transfer of WT B cells pretreated with anti-Ag IgG immune complexed Ag/CTB. We conclude that FcγRIIB expression on B cells, in addition to dendritic cells, is important for mucosal induction of Ag-specific immune tolerance.

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Regulation of allergy by Fc receptors

Cited by 92 publications

References 51 publications

Suppression of Th2-Driven Airway Inflammation by Allergen Immunotherapy Is Independent of B Cell and Ig Responses in Mice

Suppression of Th2-Driven Airway Inflammation by Allergen Immunotherapy Is Independent of B Cell and Ig Responses in Mice

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

Important Role for FcγRIIB on B Lymphocytes for Mucosal Antigen-Induced Tolerance and Foxp3+ Regulatory T Cells

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