SNORD104 MICRORNA

SNORD104 gene-encoded microRNA and its role in immune homeostasis

Coordinatore	UNIVERSITAET BERN    more  Organization address address: Hochschulstrasse 4 city: BERN postcode: 3012 contact info Titolo: Prof. Nome: Peter Matthias Cognome: Villiger Email: send email Telefono: +41 31 6328015 Fax: +41 31 6329745
Nazionalità Coordinatore	Switzerland [CH]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2012-CIG
Funding Scheme	MC-CIG
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-01-01   -   2017-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITAET BERN  Organization address address: Hochschulstrasse 4 city: BERN postcode: 3012 contact info Titolo: Prof. Nome: Peter Matthias Cognome: Villiger Email: send email Telefono: +41 31 6328015 Fax: +41 31 6329745	CH (BERN)	coordinator	100˙000.00

Mappa

 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

 Obiettivo del progetto (Objective)

'MicroRNAs constitute an essential, evolutionary conserved mechanism of posttranscriptional gene expression regulation and thereby affect almost all biological processes including immune functions. In a comprehensive small RNA profiling study we identified a new, Snord104-derived microRNA, miR-145561, which is highly expressed in activated mature lymphocytes. To investigate the role of this lymphocyte-predominant microRNA we generated miR-145561 knockout mice. Aging miR-145561-deficient mice present with splenomegaly and lymphadenopathy and show an increased frequency of germinal center B cells and memory CD4 T cells. In vitro, miR-145561-deficient B cells and T cells are hyper-responsive to innate and adaptive immune receptor stimulation. In addition, miR-145561-deficient T cells show a propensity to differentiate into IL-17 producing cells. These preliminary data strongly suggest that miR-145561 plays an essential role in immune homeostasis through its function as a non-redundant negative regulator of innate and adaptive immune receptor signaling in mature lymphocytes. The goal of the current research proposal is to investigate the function of miR-145561 in immune homeostasis and lymphocyte function through the following experimental strategy: I) identification, validation and functional evaluation of miR-145561 targets in lymphocytes; II) examination of adaptive immune responses to T cell-dependent and T cell-independent antigens in miR-145561-deficient and -proficient mice; III) investigation of the susceptibility of miR-145561-deficient mice to spontaneous autoimmunity and how miR-145561-definciency affects disease onset and severity in autoimmunity prone mice; and IV) to investigate the function of the human miR-145561 homolog. This project sheds light into the mechanisms by which microRNAs regulate immune homeostasis and contribute to the understanding of the pathogenesis of autoimmune diseases and other inflammatory disorders.'