DNGR-1 IN DCS

The dendritic cell receptor DNGR-1: Modulation of endosomal dynamics upon recognition of necrotic cells

Coordinatore	THE FRANCIS CRICK INSTITUTE LIMITED    more  Organization address address: 215 Euston Road, Gibbs Building city: LONDON postcode: NW1 2BE contact info Titolo: Ms. Nome: Heather Joanne Cognome: Woods Email: send email Telefono: 442076000000
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	221˙606 €
EC contributo	221˙606 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2012-IEF
Funding Scheme	MC-IEF
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-05-01   -   2015-04-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE FRANCIS CRICK INSTITUTE LIMITED  Organization address address: 215 Euston Road, Gibbs Building city: LONDON postcode: NW1 2BE contact info Titolo: Ms. Nome: Heather Joanne Cognome: Woods Email: send email Telefono: 442076000000	UK (LONDON)	coordinator	221˙606.40
2	CANCER RESEARCH UK  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Ms. Nome: Holly Cognome: Elphinstone Email: send email Telefono: +44 207 269 3524 Fax: +44 207 269 3585	UK (LONDON)	participant	0.00

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 Obiettivo del progetto (Objective)

'Dendritic cells (DCs) play an essential function in initiating adaptive immunity. Key to DC function are receptors for recognizing and capturing pathogens and damaged cells and for controlling subsequent antigen extraction, processing and presentation. DNGR-1 (also known as CLEC9A) is a DC-restricted C-type lectin receptor (CLR) that recognizes the actin cytoskeleton exposed on necrotic cells. DNGR-1 is not required for internalization of cell corpses by DCs but regulates their subsequent ability to crosspresent corpse-associated antigens to CD8 T-cells. The mechanisms underlying DNGR-1 function are unknown but require receptor signaling upon ligand engagement and are though to relate to modulation of endocytic traffic. Here, I hypothesize DNGR-1 promotes the stabilization of a non-degradative endo-/phagosomal compartment containing dead-cell associated cargo to permit antigen extraction from cell corpses and subsequent crosspresentation. I propose to address this hypothesis by investigating the intracellular trafficking of DNGR-1 and its ligand and the role of DNGR-1 on the endo-/phagosomal environment in DCs.'