FLAMMASEC

"Inflammasome-induced IL-1 Secretion: Route, Mechanism, and Cell Fate"

Coordinatore	KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	1˙495˙533 €
EC contributo	1˙495˙533 €
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)	2014-03-01   -   2019-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN  Organization address address: ISMANINGER STRASSE 22 city: MUENCHEN postcode: 81675 contact info Titolo: Dr. Nome: Olaf Cognome: Groß Email: send email Telefono: +49 89 4140 4874 Fax: +49 89 4140 4080	DE (MUENCHEN)	hostInstitution	1˙495˙533.00
2	KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN  Organization address address: ISMANINGER STRASSE 22 city: MUENCHEN postcode: 81675 contact info Titolo: Ms. Nome: Beate Cognome: Schaulin Email: send email Telefono: +49894140 2856 Fax: +49894140 4926	DE (MUENCHEN)	hostInstitution	1˙495˙533.00

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 Obiettivo del progetto (Objective)

'Inflammasomes are intracellular danger-sensing protein complexes that are important for host protection. They initiate inflammation by controlling the activity of the proinflammatory cytokine interleukin-1β (IL-1β). Unlike most other cytokines, IL-1β is produced and retained in the cytoplasm in an inactive pro-form. Inflammasome-dependent maturation of proIL-1β is mediated by the common component of all inflammasomes, the protease caspase-1. Caspase-1 also controls the secretion of IL-1β, but the mechanism and route of secretion are unknown. We have recently demonstrated that the ability of caspase-1 to control IL-1β secretion is not dependent on its protease activity, but rather on a scaffold or adapter function of caspase-1. Furthermore, we and others could show that caspase-1 can control the secretion of non-substrates like IL-1α. These insights provide us with new and potentially revealing means to investigate the downstream effector functions of caspase-1, including the route and mechanism of IL-1 secretion. We will develop new tools to study the process of IL-1 secretion by microscopy and the novel mode-of-action of caspase-1 through the generation of transgenic models. Despite the important role of IL-1 in host defence against infection, dysregulated inflammasome activation and IL-1 production has a causal role in a number of acquired and hereditary auto-inflammatory conditions. These include particle-induced sterile inflammation (as is seen in gout and asbestosis), hereditary periodic fever syndromes, and metabolic diseases like diabetes and atherosclerosis. Currently, recombinant proteins that block the IL-1 receptor or deplete secreted IL-1 are used to treat IL-1-dependent diseases. These are costly treatments, and are also therapeutically cumbersome since they are not orally available. We hope that a better understanding of caspase-1-mediated secretion of IL-1 will unveil mechanisms that may serve as targets for future therapies for these diseases.'