Expression of High-Affinity IgE Receptor (Fc&amp;#949;RI) on Human Alveolar Macrophages from Atopic and Non-Atopic Patients

Ochiai, Kenichi; Kagami, M; Umemiya, K; Matsumura, Ryutaro; Kawashima, Tatsuo; Tomioka, Hisao

doi:10.1159/000237417

Cited by 11 publications

(6 citation statements)

References 5 publications

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“…These data also suggest that all three subunits of FcεRI were simultaneously transcribed. Using reverse transcription (RT‐PCR), the similar mRNA expression for FcεRI subunits has been observed in isolated human alveolar macrophages 24 or eosinophils 10 . Although chimeric receptor consisting of αγ 2 had a similar function to the native FcεRI (αβγ 2 ), 25 it has been demonstrated that the γ‐dimer functions as an autonomous activation module, while β‐functions as a signal amplifier providing a gain of 5‐ to 7‐fold for Syk activation and calcium mobilization 26 …”

Section: Discussionmentioning

confidence: 77%

High‐affinity immunoglobulin E receptor (FcεRI)‐bearing eosinophils, mast cells, macrophages and Langerhans’ cells in allergen‐induced late‐phase cutaneous reactions in atopic subjects

et al. 1998

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SUMMARYWe have used in situ hybridization (ISH ) and immunohistochemistry (IHC ) to investigate the kinetics of the expression for FceRI mRNA (a-, b-and c-chains), the a-chain protein product, as well as the phenotype of the mRNA-or protein-positive cells in allergen-induced late-phase skin reactions in atopic subjects. Compared with diluent controls, there were significant increases in the total numbers of mRNA+ cells for the a-, b-and c-chains for FceRI at all time-points (6, 24 and 48 hr) after allergen challenge (P<0·01). By double IHC/ISH significant increases in a-, band c-chain mRNA+ macrophages, eosinophils, mast cells and CD1a+ cells were also observed after allergen challenge (P<0·05). The distribution of FceRI subunit (a-, b-, or c-chain) mRNA+ co-localization was CD68+ macrophages (42-47%), EG2+ eosinophils (33-39%), tryptase+ mast cells (5-11%) and CD1a+ Langerhans' cells (2-4%). Using single IHC, significant increases in the total number of FceRI protein+ cells (P<0·01) were observed 24 and 48 hr after allergen challenge. Double IHC showed that the distribution of FceRI+ cells was tryptase+ mast cells (33%), CD68+ macrophages (36%), EG2+ eosinophils (20%), CD1a+ Langerhans' cells (4%) and unidentified cells (7%), at the 24-hr allergen-challenged sites. These observations suggest that the cutaneous late-phase reaction in man is associated with up-regulation of FceRI on eosinophils, macrophages, mast cells and Langerhans' cells.

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Section: Discussionmentioning

confidence: 77%

High‐affinity immunoglobulin E receptor (FcεRI)‐bearing eosinophils, mast cells, macrophages and Langerhans’ cells in allergen‐induced late‐phase cutaneous reactions in atopic subjects

et al. 1998

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“…These events can lead to a domino effect where more IgE produced by B cells may become involved in forming more immune complexes resulting in further exacerbation of airway inflammation. Second, Fc⑀RI is expressed by some types of APC, including monocytes (35), dendritic cells (36), and alveolar macrophages (37), and the IgE immune complexes may be more readily captured by these cells and processed for Ag presentation. Our results with Fc⑀RI-deficient mice indeed support a critical role for Fc⑀RI in the augmented responses induced by IgE immune complexes.…”

Section: Discussionmentioning

confidence: 99%

Role for IgE in Airway Secretions: IgE Immune Complexes Are More Potent Inducers Than Antigen Alone of Airway Inflammation in a Murine Model

Zuberi

Apgar

Chen

et al. 2000

The Journal of Immunology

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IgE is present in airway secretions from human patients with allergic rhinitis and bronchial asthma. However, the contribution of IgE present locally to the overall airway inflammation is not well understood. We hypothesize that Ag-specific IgE can capture airborne Ags and form immune complexes. These immune complexes may function as potent inducers of immune responses in the lung, contributing to the perpetuation of airway inflammation. BALB/c mice were first sensitized with OVA in alum systemically and then challenged with nebulized OVA. Bronchoalveolar lavage (BAL) fluid from these mice contained significant amounts of IgE, of which >50% was Ag specific. The IgE levels in airway secretions remained elevated for more than 15 days after the termination of Ag exposure. Significant amounts of IgE-OVA immune complexes were detected in BAL fluid from the OVA-challenged mice. For comparison of IgE immune complexes vs Ag alone, we treated OVA-immunized mice with intranasal administration of trinitrophenyl-OVA or trinitrophenyl-OVA-anti-DNP IgE. Those treated with the immune complexes showed significantly higher levels of IL-4 and more pronounced eosinophilia in BAL fluid than did those receiving the Ag alone. The IgE immune complexes did not augment the inflammatory response in high affinity IgE receptor (FcεRI)-deficient mice. We conclude that IgE present in the airways can capture the Ag and that the immune complexes thus formed may augment allergic airway response in an FcεRI-dependent manner. Thus, IgE present in airway secretions may facilitate Ag-mediated allergic airway inflammation.

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“…FcεRI(αγ) are expressed by human alveolar macrophage in asthmatic patients (22). We therefore examined FcγRIV on mouse alveolar macrophages.…”

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

confidence: 99%

“…Although hFcεRI has a high affinity whereas mFcγRIV has a low affinity for IgE, both can be engaged by IgE ICs. Moreover, hFcεRI is expressed without FcRβ in macrophages and neutrophils and especially in atopic patients (13,22). Mouse macrophage/neutrophil FcγRIV and human macrophage/neutrophil FcεRI(αγ) therefore have the same quaternary structure: an IgE-binding subunit and the same ITAMcontaining FcRγ subunit.…”

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.

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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Expression of High-Affinity IgE Receptor (FcεRI) on Human Alveolar Macrophages from Atopic and Non-Atopic Patients

Cited by 11 publications

References 5 publications

High‐affinity immunoglobulin E receptor (FcεRI)‐bearing eosinophils, mast cells, macrophages and Langerhans’ cells in allergen‐induced late‐phase cutaneous reactions in atopic subjects

High‐affinity immunoglobulin E receptor (FcεRI)‐bearing eosinophils, mast cells, macrophages and Langerhans’ cells in allergen‐induced late‐phase cutaneous reactions in atopic subjects

Role for IgE in Airway Secretions: IgE Immune Complexes Are More Potent Inducers Than Antigen Alone of Airway Inflammation in a Murine Model

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

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