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    more 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

#	participant	country	role	EC contrib. [€]
1	HELMHOLTZ-ZENTRUM FUER INFEKTIONSFORSCHUNG GMBH  Organization address address: Inhoffenstrasse 7 city: BRAUNSCHWEIG postcode: 38124 contact info Titolo: Dr. Nome: Michael Cognome: Straetz Email: send email Telefono: +49 531 61812020 Fax: +49 531 61812299	DE (BRAUNSCHWEIG)	beneficiary	424˙632.00
2	UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF  Organization address address: Martinistrasse 52 city: HAMBURG postcode: 20246 contact info Titolo: Dr. Nome: Samuel Cognome: Huber Email: send email Telefono: +49 40 741057273 Fax: +49 40 7410 59038	DE (HAMBURG)	hostInstitution	1˙073˙760.00
3	UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF  Organization address address: Martinistrasse 52 city: HAMBURG postcode: 20246 contact info Titolo: Ms. Nome: Karin Cognome: Hansen Email: send email Telefono: +49 40 7410 58653 Fax: +49 40 7410 40156	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.'