CLR SENSING NECROSIS

Immune Functions of Myeloid Syk-coupled C-type Lectin Receptors Sensing Necrosis

 Coordinatore  

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Non specificata
 Totale costo 1˙297˙671 €
 EC contributo 1˙297˙671 €
 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-2010-StG_2009
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-12-01   -   2016-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III

 Organization address address: C/ MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029

contact info
Titolo: Dr.
Nome: David
Cognome: Sancho Madrid
Email: send email
Telefono: +34 914531200
Fax: +34 914531245

ES (MADRID) hostInstitution 1˙297˙671.00
2    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III

 Organization address address: C/ MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029

contact info
Titolo: Ms.
Nome: Luzma
Cognome: Garcia Piqueres
Email: send email
Telefono: +34 91 453 1200
Fax: +34 91 453 1245

ES (MADRID) hostInstitution 1˙297˙671.00

Mappa


 Word cloud

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

syk    pathologies    recognition    diseases    sensing    mechanisms    clrs    immunity    dectin    necrotic    trigger    induce    cells    coupled    adaptive    myeloid    receptors    necrosis    immune    cell    dc    macrophages    clec   

 Obiettivo del progetto (Objective)

'Necrosis triggers an inflammatory response driven by macrophages that normally contributes to tissue repair but, under certain conditions, can induce a state of chronic inflammation that forms the basis of many diseases. In addition, dendritic cell (DC)-mediated presentation of antigens from necrotic cells can trigger adaptive immunity in infection-free situations, such as autoimmunity or therapy-induced tumour rejection. Recently, we and others have identified the myeloid C-type lectin receptors (CLRs) CLEC9A (DNGR-1), in DC, and Mincle, in macrophages, as receptors for necrotic cells that can signal via the Syk kinase. Previous studies on similar Syk-coupled CLRs showed that Dectin-1 and Dectin-2 can induce innate and adaptive immune responses. We thus hypothesise that recognition of cell death by myeloid Syk-coupled CLRs is at the root of immune pathologies associated with accumulation of dead cells. The overall objective of this proposal is to investigate necrosis sensing by myeloid cells as a trigger of immunity and to study the underlying molecular mechanisms. Our first goal is to characterise signalling and gene induction via CLEC9A as a model necrosis receptor in DCs. Second, we will investigate the role of myeloid Syk-coupled necrosis-sensing CLRs in animal models of atherosclerosis, lupus and immunity to chemotherapy-treated tumours. Our preliminary data suggest that additional receptors can couple necrosis recognition to the Syk pathway in DC; thus, our third aim is to identify novel myeloid Syk-coupled receptors for necrotic cells. Characterisation of the outcomes of sensing necrosis by myeloid Syk-coupled receptors and their effect on the proposed pathologies promises to identify new mechanisms and targets for the treatment of these diseases.'

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