SNORD104 MICRORNA
SNORD104 gene-encoded microRNA and its role in immune homeostasis
| Coordinatore | UNIVERSITAET BERN
Organization address
address: Hochschulstrasse 4 contact info |
| 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
| # | ||||
|---|---|---|---|---|
| 1 |
UNIVERSITAET BERN
Organization address
address: Hochschulstrasse 4 contact info |
CH (BERN) | coordinator | 100˙000.00 |
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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.'