EGF-R FOR IMMUNITY

Use of EGF-R antagonists for the treatment of chronic infections and tumor growth

 Coordinatore THE UNIVERSITY OF EDINBURGH 

 Organization address address: OLD COLLEGE, SOUTH BRIDGE
city: EDINBURGH
postcode: EH8 9YL

contact info
Titolo: Ms.
Nome: Angela
Cognome: Noble
Email: send email
Telefono: 441317000000
Fax: 441317000000

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-2013-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-03-01   -   2018-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF EDINBURGH

 Organization address address: OLD COLLEGE, SOUTH BRIDGE
city: EDINBURGH
postcode: EH8 9YL

contact info
Titolo: Ms.
Nome: Angela
Cognome: Noble
Email: send email
Telefono: 441317000000
Fax: 441317000000

UK (EDINBURGH) coordinator 100˙000.00

Mappa


 Word cloud

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

tumor    cell    function    therapy    act    amphiregulin    cells    functionality    therapeutic    egf    determine    virus    induced    effect    regulated    tolerance    regulatory    inhibitor    immune   

 Obiettivo del progetto (Objective)

'FoxP3 expressing regulatory T-cells play an important role in the induction of peripheral tolerance and the prevention of auto-immune responses. How the functionality of regulatory T-cells is regulated at the site of inflammation remains poorly understood. We just recently discovered that the functionality of regulatory T-cells is regulated via the EGF-R that is expressed by activated regulatory T-cells. In in vitro suppression assays the presence of the EGF-like growth factor Amphiregulin significantly enhanced the suppressive capacity of regulatory T-cells and, in vivo, Amphiregulin-induced signals enabled regulatory T-cells to induce tolerance against innocuous antigens. This effect was blocked upon application of EGF-R antagonists (Zaiss et al. 2013). Based on these findings, the objectives of this proposal are: 1.a) To determine the role of regulatory T-cells during tumor therapy; in specific during induced lymphopenia in the context of adoptive cell transfer (ACT) based tumor therapy. 1.b) To determine whether EGF-R inhibitors can suppress regulatory T-cell function such that they enhance the efficacy of ACT based tumor therapy? 2) To determine whether smallpox viruses use their virus-encoded EGF-like growth factors to enhance regulatory T-cell function, and thus as an immune escape mechanism? This will answer the question whether interference with regulatory T-cell function explains for the immune-stimulatory effect of EGF-R inhibitor treatment, during vaccinia virus infections. 3) To determine whether we can develop an EGF-R inhibitor that selectively targets regulatory T-cells, and thus keeps all other functions of the EGF-R, for example in tissue homeostasis, intact?

Taken together, this proposed project tests a novel therapeutic approach by which we expect to have hit a so far unrecognized, therapeutic “Achilles’ heel” of Tregs, i.e. via the regulation of Treg functionality by EGF-R ligands.'

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