ATHEROMOTO

Vascular inflammation and atherosclerosis

Coordinatore	INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)    more  Organization address address: 101 Rue de Tolbiac city: PARIS postcode: 75654 contact info Titolo: Prof. Nome: Thierry Cognome: Couffinhal Email: send email Telefono: 33557891979 Fax: -+33 5 56 36 89 79
Nazionalità Coordinatore	France [FR]
Totale costo	0 €
EC contributo	239˙551 €
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-IEF-2008
Funding Scheme	MC-IEF
Anno di inizio	2009
Periodo (anno-mese-giorno)	2009-09-01   -   2011-08-31

 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: Prof. Nome: Thierry Cognome: Couffinhal Email: send email Telefono: 33557891979 Fax: -+33 5 56 36 89 79	FR (PARIS)	coordinator	239˙551.42

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 Obiettivo del progetto (Objective)

'Atherosclerosis is an immunoinflammatory disease of the arterial wall that carries an important socio-economic burden. Atherosclerotic lesions contain activated T cells and specific cytokines along with immunoglobulins. Several studies have shown that atherosclerotic patients develop a perturbed inflammation toward arterial proteins suggesting that autoimmune processes may play a role in atherosclerosis progression. Moreover, patients with aggressive inflammatory diseases such as autoimmune diseases, including SLE, rheumatoid arthritis and type I diabetes, exhibit a higher incidence of atherosclerosis and are at significant risk of premature cardiovascular disease. The continued emergence of cardiovascular diseases and accelerated atherosclerosis in a wide variety of autoantibody-driven diseases emphasizes the need to identify early diagnostic markers and immunotherapeutic targets for the treatment of these complications. The specific hypothesis is that the initiation and progression of atherosclerosis is regulated by autoantibodies directed toward vascular wall components, defects in immune complex (IC) and autoantibody clearance. Our long term goal is to understand the cellular and humoral immunity/autoimmunity basis of atherosclerosis. We will focus our study on analyzing the inhibitory Fc type IIB receptor of immunoglobulin G (FcgRIIB) for the creation of the mouse line of autoimmunity. FcgRIIB is critical in controlling excessive antibody production by B lymphocytes, regulating macrophage reactivity and controlling autoimmunity. We propose to modulate the expression of this “suppressor” of autoimmunity in a hyperlipidemic mouse background. Our specific aims are: Aim I- To create a mouse model that combines of autoimmunity and hypercholesterolemia by silencing the FcgRIIB gene expression in LDLR-/- mouse background. Aim II- To identify panels of antigens that elicit an autoimmune response in this mouse model using a proteomic approach.'