DAMAGECONTROL
Tissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
| Coordinatore | FUNDACAO CALOUSTE GULBENKIAN
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Portugal [PT] |
| Totale costo | 2˙306˙196 € |
| EC contributo | 2˙306˙196 € |
| Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | ERC-2011-ADG_20110310 |
| Funding Scheme | ERC-AG |
| Anno di inizio | 2012 |
| Periodo (anno-mese-giorno) | 2012-04-01 - 2017-03-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
FUNDACAO CALOUSTE GULBENKIAN
Organization address
address: AVENIDA DE BERNA 45A contact info |
PT (LISBOA) | hostInstitution | 2˙306˙196.80 |
| 2 |
FUNDACAO CALOUSTE GULBENKIAN
Organization address
address: AVENIDA DE BERNA 45A contact info |
PT (LISBOA) | hostInstitution | 2˙306˙196.80 |
Mappa
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Obiettivo del progetto (Objective)
'We propose to study evolutionarily conserved stress-responsive protective mechanisms that limit the extent of tissue damage caused by pathogens or by the innate as well as adaptive immune response elicited by those pathogens, which, without a countervailing response would lead to irreversible tissue damage and disease. We refer to these protective mechanisms as “tissue damage control”, and will argue they are an essential component of immunity that allows the effector mechanisms involved in pathogen clearance to operate without causing disease. This proposal aims at identifying and characterizing the mechanism of action of stress-induced genetic programs conferring tissue damage control and to relate those to the pathogenesis of different immune mediated inflammatory diseases. We hypothesize that these genetic programs share as a common denominator their regulation by a restricted number of evolutionary conserved transcription factors that act as “master regulators” of different protective responses to specific forms of stress. We will use “loss” and “gain” of function approaches targeting these master regulators in mice to characterize their function and identify stress-responsive genes conferring tissue metabolic adaptation, cytoprotection and/or tissue regeneration, all of which are components of tissue damage control. Expression of these master regulators likely impacts the pathogenesis of immune mediated inflammatory conditions, as tested under this proposal for infectious as well as autoimmune-like diseases. This proposal should unveil an essential component of immunity that uncouples pathogen clearance from tissue damage and disease, namely tissue damage control, providing new therapeutic targets to suppress the pathogenesis of a broad range of immune mediated inflammatory diseases.'