TCONTREGAPOAI

Apolipoprotein A-I and modulation of T cell functions

Coordinatore	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE    more  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Renata Cognome: Schaeffer Email: send email Telefono: 441223000000 Fax: 441223000000
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	231˙283 €
EC contributo	231˙283 €
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)	2013-05-03   -   2015-05-02

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Ms. Nome: Renata Cognome: Schaeffer Email: send email Telefono: 441223000000 Fax: 441223000000	UK (CAMBRIDGE)	coordinator	231˙283.20

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 Obiettivo del progetto (Objective)

'The pathogenesis of atherosclerosis involves inflammation and immune reactions. T cell responses contribute to local inflammation and growth of the atherosclerotic plaque. As intensified inflammatory activation may lead to local proteolysis, plaque rupture, and formation of a thrombus, studies of conventional and regulatory T cell functions during hypercholesterolemia are of outmost importance. Low levels of high-density lipoprotein (HDL) cholesterol are associated with inflammatory and immune disorders, including atherosclerosis. Although accumulating evidence suggests that HDL has anti-inflammatory properties, and functions as a part of the immune system, the mechanisms by which HDL inhibits atherosclerosis are not yet fully understood. Here, I propose to study the potential role of apoA-I in regulating the function of conventional and regulatory T cells. To this end, I will use hypercholesterolemic LDL receptor (LDLr) -/- and apoA-I-/- double knock-out (DKO) mice that develop severe atherosclerosis and display autoimmune phenotype, and, as a control, (LDLr) -/- single knock-out (SKO) mice fed atherogenic diet to study: 1) the role of apoA-I in regulating T cell motility, 2) the influence of apoAI on adhesion of T cells to antigen-presenting cells, 3) the effect of apoA-I on T-cell signaling molecules that regulate T cell motility and adhesion, 4) the relation between apoA-I and apoA-I-affected T-cell signaling molecules in vivo. These complementary approaches will allow me to investigate the role of apoA-I on regulating T cells functions, and will be indispensable to assess an impact of apoA-I-affected T-cell signaling molecules on atherosclerosis and autoimmune diseases. As conventional T cells critically modulate atherosclerosis by promoting inflammation, and regulatory T cells display atheroprotective properties, mechanistic insights into how apoA-I regulates T cell functions will advance our understanding of the immune processes involved in atherosclerosis.'