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FcgammaRIV is a mouse IgE receptor that resembles macrophage FcepsilonRI in humans and promotes IgE-induced lung inflammation.
Mancardi D. A., Iannascoli B., Hoos S., England P., Daëron M., Bruhns P.
Journal of Clinical Investigation 118, 11 (2008) 3738-50 - http://hal-pasteur.archives-ouvertes.fr/pasteur-00363913
(18949059)
FcgammaRIV is a mouse IgE receptor that resembles macrophage FcepsilonRI in humans and promotes IgE-induced lung inflammation.
David A. Mancardi1, Bruno Iannascoli1, Sylviane Hoos2, Patrick England3, Marc Daëron1, Pierre Bruhns () 1
1 :  Allergologie Moléculaire et Cellulaire
INSERM : U760 – Institut Pasteur de Paris
25-28, rue du Docteur Roux F-75724 PARIS CEDEX 15
France
2 :  Département de Biologie Structurale et Chimie, Plateforme de Biophysique des Macromolécules et de leurs Interactions
CNRS : URA2185
Institut Pasteur 25-28, rue du Docteur Roux 75724 Paris Cedex 15
France
3 :  Département de Biologie Structurale et Chimie, Plateforme de Biophysique des Macromolécules et de leurs Interactions
CNRS : URA2185
Institut Pasteur 25-28, rue du Docteur Roux 75724 Paris Cedex 15
France
FcgammaRIV 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 mFcgammaRIV. Although little is known about mFcgammaRIV, it has been proposed to be the mouse homolog of human FcgammaRIIIA (hFcgammaRIIIA) because of high sequence homology. Our work, however, has revealed what we believe to be new properties of mFcgammaRIV 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 mFcgammaRIV functioned as a high-affinity IgG receptor, mFcgammaRIV-bound monomeric IgGs were readily displaced by IgE immune complexes. Engagement of mFcgammaRIV by IgE immune complexes induced bronchoalveolar and peritoneal macrophages to secrete cytokines, suggesting that mFcgammaRIV may be an equivalent of human FceRI(alphagamma), which is expressed by macrophages and neutrophils and especially in atopic individuals, rather than an equivalent of hFcgammaRIIIA, which has no affinity for IgE. Using mice lacking 3 FcgammaRs and 2 FceRs and expressing mFcgammaRIV only, we further demonstrated that mFcgammaRIV 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 mFcgammaRIV-expressing lung cells. We therefore suggest that a similar cooperation may occur between mast cells and hFceRI-expressing lung cells in human allergic asthma.
Sciences du Vivant/Immunologie/Allergologie
Anglais
0021-9738

Articles dans des revues avec comité de lecture
10.1172/JCI36452
Journal of Clinical Investigation (J Clin Invest)
Publisher American Society for Clinical Investigation
ISSN 0021-9738 
internationale
11/2008
23/10/2008
118
11
3738-50

Animals – Bone Marrow Cells – Cell Line – Humans – Immunoglobulin E – Inflammation – Kidney – Lung – Macrophages – Mice – Inbred C57BL – Knockout – Receptors – IgE – IgG – Animals
This work was supported by the Institut Pasteur and INSERM and by grants from Agence Nationale de la Recherche (ANR) (05-JCJC-0236-01), Fondation pour la Recherche Médicale (FRM) (Défis de la Recherche en Allergologie), and the MUGEN European Network of Excellence
Référence du projet ANR-05-JCJC-0236
Année 2005
Acronyme du projet FcR & Allergy
Titre du projet Roles and interactions of human FcR in allergic symptoms induced by human immunoglobulins and allergens: construction of a "humanized" mouse model.
Intitulé Jeunes chercheuses et jeunes chercheurs
Acronyme de l'appel JCJC
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