AHRIMMUNITY
The influence of Aryl hydrocarbon receptor ligands on protective and pathological immune responses
| Coordinatore | MEDICAL RESEARCH COUNCIL
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | United Kingdom [UK] |
| Totale costo | 1˙242˙351 € |
| EC contributo | 1˙242˙351 € |
| 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-2008-AdG |
| Funding Scheme | ERC-AG |
| Anno di inizio | 2009 |
| Periodo (anno-mese-giorno) | 2009-02-01 - 2014-01-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
CHRISTIAN-ALBRECHTS-UNIVERSITAET ZU KIEL
Organization address
address: OLSHAUSENSTRASSE 40 contact info |
DE (KIEL) | beneficiary | 479˙636.40 |
| 2 |
TURUN YLIOPISTO
Organization address
address: YLIOPISTONMAKI contact info |
FI (TURUN YLIOPISTO) | beneficiary | 40˙316.40 |
| 3 |
MEDICAL RESEARCH COUNCIL
Organization address
address: NORTH STAR AVENUE POLARIS HOUSE contact info |
UK (SWINDON) | hostInstitution | 722˙398.80 |
| 4 |
MEDICAL RESEARCH COUNCIL
Organization address
address: NORTH STAR AVENUE POLARIS HOUSE contact info |
UK (SWINDON) | hostInstitution | 722˙398.80 |
Mappa
Word cloud
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
Obiettivo del progetto (Objective)
'The Aryl hydrocarbon receptor is an evolutionary conserved widely expressed transcription factor that mediates the toxicity of a substantial variety of exogenous toxins, but is also stimulated by endogenous physiological ligands. While it is known that this receptor mediates the toxicity of dioxin, this is unlikely to be its physiological function. We have recently identified selective expression of AhR in the Th17 subset of effector CD4 T cells. Ligation of AhR by a candidate endogenous ligand (FICZ) which is a UV metabolite of tryptophan causes expansion of Th17 cells and the induction of IL-22 production. As a consequence, AhR ligation will exacerbate autoimmune diseases such as experimental autoimmune encephalomyelitis. Little is known so far about the impact of AhR ligands on IL-17/IL-22 mediated immune defense functions. IL-22 is considered a pro-inflammatory Th17 cytokine, which is involved in the etiology of psoriasis, but it has also been shown to be a survival factor for epithelial cells. AhR is polymorphic and defined as high or low affinity receptor for dioxin leading to the classification of high and low responder mouse strains based on defined mutations. In humans similar polymorphisms exist and although on the whole human AhR is thought to be of low affinity in humans, there are identified mutations that confer high responder status. No correlations have been made with Th17 mediated immune responses in mice and humans. This study aims to investigate the role of AhR ligands and polymorphisms in autoimmunity as well as protective immune responses using both mouse models and human samples from normal controls as well as psoriasis patients.'