IL-22 AND IL-22BP
Identifying the immune and microbial network controlling the IL-22 – IL-22bp axis to open the doors for targeted therapies
| Coordinatore | UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Germany [DE] |
| Totale costo | 1˙498˙392 € |
| EC contributo | 1˙498˙392 € |
| 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-2013-StG |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2014 |
| Periodo (anno-mese-giorno) | 2014-01-01 - 2018-12-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
HELMHOLTZ-ZENTRUM FUER INFEKTIONSFORSCHUNG GMBH
Organization address
address: Inhoffenstrasse 7 contact info |
DE (BRAUNSCHWEIG) | beneficiary | 424˙632.00 |
| 2 |
UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF
Organization address
address: Martinistrasse 52 contact info |
DE (HAMBURG) | hostInstitution | 1˙073˙760.00 |
| 3 |
UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF
Organization address
address: Martinistrasse 52 contact info |
DE (HAMBURG) | hostInstitution | 1˙073˙760.00 |
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Obiettivo del progetto (Objective)
'Chronic mucosal inflammation and tissue damage predisposes patients to the development of colorectal cancer. One hypothesis is that the same factors important for wound healing, if left unchecked, also promote tumorigenesis. Tight control by a sensor of tissue damage should induce these factors to promote tissue repair, while limiting their activity to prevent development of cancer. IL-22, a prototypical tissue repair factor, plays an important role in a wide variety of intestinal disease including infection, wound healing, colitis, and cancer. Indeed, IL-22 has protective and detrimental effects dependent on the milieu and disease suggesting that proper regulation is required. IL-22 expression is directly regulated, additionally a soluble IL-22 receptor (IL-22 binding protein; IL-22bp), can bind and neutralize IL-22. We reported recently that sensing of intestinal tissue damage and components of the microbiota via the NLRP3 or NLRP6 inflammasomes led to a down regulation of IL-22bp, thereby increasing bioavailability of IL-22. IL-22, which is induced during intestinal tissue damage, exerted protective properties during the peak of damage, but promoted tumor development if not controlled by IL-22bp during the recovery phase. Accordingly a spatial and temporal regulation of IL-22 is crucial. Hence, global administration or blockade of IL-22 is unlikely to be therapeutically beneficial. We are using several newly generated conditional knock-out (cCasp1-/-, cIL-18R-/-, cIL-18-/-, cIL-22R1-/-), knock-in (IL-22 BFP), and gnotobiotic mice, aiming to analyze the cellular and microbial network regulating the IL-22 – IL-22bp axis at a resolution previously unfeasible. Our results will provide novel insights into the network between microflora, epithelium, and immune system regulating tissue regeneration and tumor development, and can lead to therapies for potentially a wide variety of intestinal diseases, such as infection, colon cancer, IBD, or wound healing.'