MYELOSHOCK

"Role of myeloid cells, their mediators and their antibody receptors in allergic shock (anaphylaxis) using humanized mouse models and clinical samples"

 Coordinatore INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM) 

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 Nazionalità Coordinatore France [FR]
 Totale costo 1˙999˙704 €
 EC contributo 1˙999˙704 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2013-CoG
 Funding Scheme ERC-CG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-09-01   -   2019-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)

 Organization address address: 101 Rue de Tolbiac
city: PARIS
postcode: 75654

contact info
Titolo: Dr.
Nome: Pierre
Cognome: Bruhns
Email: send email
Telefono: +33 145688629
Fax: +33 140613160

FR (PARIS) hostInstitution 1˙999˙704.00
2    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)

 Organization address address: 101 Rue de Tolbiac
city: PARIS
postcode: 75654

contact info
Titolo: Ms.
Nome: Laurie
Cognome: Louis-Joseph
Email: send email
Telefono: +33 1 45 17 29 32
Fax: +33 1 45 17 29 11

FR (PARIS) hostInstitution 1˙999˙704.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

shock    patients    reactions    human    responsible    receptors    release    mice    reaction    anaphylactic    clinical    drug    igg    models    induced    cells    establishing    allergen    anaphylaxis    reported    ige    mast    rely   

 Obiettivo del progetto (Objective)

'Anaphylaxis is a hyperacute allergic reaction of increasing incidence that can be of fatal consequence and that has no specific treatment. Anaphylaxis is thought to rely on mechanisms involving mast cells that bear allergen-specific IgE and that release histamine when encountering allergen. Clinical cases, however, report anaphylaxis in the absence of specific IgE or medical history of allergy. We reported that murine models of anaphylaxis rely on IgG, rather than on IgE, that enable neutrophils, monocytes and basophils, rather than mast cells, to release Platelet Activating Factor following engagement of their IgG receptors. Supporting these findings, allergen-specific IgG are found in anaphylactic patients, and we reported that anaphylaxis in mice expressing a human IgG receptor relies also on circulating myeloid cells.

We aim at unravelling the parameters that control anaphylaxis in a novel clinically-relevant model of drug-induced anaphylaxis, strengthened by human-based studies involved patients undergoing drug-induced anaphylaxis in collaboration with clinicians and, altogether, rethink the principles of anaphylaxis. Do allergen-specific IgG concur to anaphylaxis in humans? Do these IgG antibodies regulate IgE-induced reactions? Which IgG receptors are involved? In which tissue does the anaphylactic reaction start? Which cell type(s) are responsible? Among the mediators that are released, which ones are responsible for the shock? Can an anaphylactic reaction be stopped specifically for an allergen? We propose to address these questions by exploiting humanized mice we obtained and by establishing novel models, by visualizing anaphylactic reactions in real time in vivo, by dissecting the cascade of events leading to the shock. Finally, we aim at establishing the proof of concept of allergen capture/encapsulation and propose the first allergen-specific strategy for treating the life-threatening clinical situation that represents drug-induced anaphylaxis.'

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MOLECMAP (2012)

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OECUMENE (2010)

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CARCHIPELAGO (2013)

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