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miRNAs in TH2 cells

Role of extracellular miRNAs in T cell development, TH2 cell differentiation and TH2 cell-mediated effector function

Total Cost €

0

EC-Contrib. €

0

Partnership

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Project "miRNAs in TH2 cells" data sheet

The following table provides information about the project.

Coordinator
THE FRANCIS CRICK INSTITUTE LIMITED 

Organization address
address: 1 MIDLAND ROAD
city: LONDON
postcode: NW1 1AT
website: www.crick.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Project website https://www.crick.ac.uk/
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-08-01   to  2017-07-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE FRANCIS CRICK INSTITUTE LIMITED UK (LONDON) coordinator 183˙454.00
2    MEDICAL RESEARCH COUNCIL UK (SWINDON) participant 0.00

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 Project objective

It is estimated that more than 200 million Europeans suffer from at least one type of allergy. This condition is elicited by an hyper-activated type-2 inflammatory response coordinated by T helper (TH)-2 cells. In spite a good insight into the molecular mechanisms that triggers TH2 cells activation, the lack in understanding their post-transcriptional regulation is hampering the access to new potential therapeutic targets to curtail the allergy epidemic. Micro-RNA (miRNAs) are regulatory molecules essential for life, which play a fundamental role in shaping cellular functions via post-transcriptional repression of the cellular transcriptome. Though previously considered to operate exclusively inside the parent cell, it is now acknowledged that miRNAs can exit cellular boundaries and control transcription in bystander cells. We recently reported that regulatory T (TREG) cells secret specific miRNAs to repress TH1 cell-mediated immunopathology, and ameliorate a mouse model of autoimmune disease. In this proposal, we will address the role of extracellular miRNAs for the normal T cell development and during allergic inflammation of the airways. To this end, we produced a novel animal model that allows - for the first time - to selectively ablate the activity of extracellular miRNAs in T cells. We will use biochemical, RNA-sequencing and bioinformatics analysis to identify the molecular mechanisms for miRNAs sorting to exocytosis and to identify the miRNAs transferred to and from TH2 cells. This proposal will significantly expand our understanding of transferred miRNAs in the contest of health and disease, and will uncover novel cellular pathways to exploit as therapeutic targets.

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The information about "MIRNAS IN TH2 CELLS" are provided by the European Opendata Portal: CORDIS opendata.

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