NKG2D-IMMUNO

The role of NKG2D in CD4+ T cell function and autoimmunity

Coordinatore	Deutsches Rheuma-Forschungszentrum Berlin    more  Organization address address: Chariteplatz 1 city: Berlin postcode: 10117 contact info Titolo: Mrs. Nome: Petra Cognome: Starke Email: send email Telefono: 493028000000
Nazionalità Coordinatore	Germany [DE]
Totale costo	168˙794 €
EC contributo	168˙794 €
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   -   2016-06-21

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	Deutsches Rheuma-Forschungszentrum Berlin  Organization address address: Chariteplatz 1 city: Berlin postcode: 10117 contact info Titolo: Mrs. Nome: Petra Cognome: Starke Email: send email Telefono: 493028000000	DE (Berlin)	coordinator	168˙794.40

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 Obiettivo del progetto (Objective)

'More than 5 million people in Europe live with inflammatory bowel disease (IBD) or rheumatoid arthritis (RA). Both diseases are characterized by chronic inflammation partially mediated by inappropriate T cell response. Effector T-cell responses can be modulated by competing positive or negative costimulatory signals, and dysregulated balance between these signals may lead to chronic autoimmune inflammation. In mice, within the CD4 T cell population, the expression of NKG2D is primarily associated with pathological conditions and the administration of blocking anti-NKG2D antibodies ameliorated the disease in mouse models of arthritis and IBD. Therefore the aim of my project proposal is to clarify the role of NKG2D receptor signalling in CD4 T cell biology and in the pathogenesis of autoimmune diseases. My work will implement mouse models to study the specific impact of NKG2D expressed on CD4 T cells in the priming, formation and maintainance of memory of CD4 T cells and their cytokine profile during homeostasis as well as in preclinical models of IBD and RA. Moreover, by global analysis of human NKG2D CD4 T cells from the sites of inflammation, we aim to better understand the possible role of NKG2D in driving inflammatory responses in IBD and RA patients. By combining these approaches, we intend to get further insights into the role of NKG2D in the regulation of autoimmune diseases and to identify strategies to possibly ameliorate tissue damage and dampen inflammation.'