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Kidney-Treg SIGNED

Characterisation and impact of kidney-resident Tregs in kidney physiology and pathologies

Total Cost €

0

EC-Contrib. €

0

Partnership

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Project "Kidney-Treg" data sheet

The following table provides information about the project.

Coordinator
THE BABRAHAM INSTITUTE 

Organization address
address: Babraham Hall
city: CAMBRIDGE
postcode: CB22 3AT
website: www.babraham.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]
 Total cost 224˙933 €
 EC max contribution 224˙933 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2022-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE BABRAHAM INSTITUTE UK (CAMBRIDGE) coordinator 224˙933.00

Map

 Project objective

Tregs are a subtype of T cells exerting immunosuppressive functions that are vital to prevent autoimmunity. Recently, tissue-resident Tregs have been proposed to be phenotypically and functionally distinct from the generic Tregs in circulation. Systemic Treg supplementation and depletion studies strongly support a role for Tregs in protection from injury and promotion of tissue repair in models of kidney diseases, highlighting the potential of harnessing Tregs in these pathologies. However, due to the systemic nature of the Treg manipulation in these studies, it is unknown if the effect resides in systemic impacts or in tissue-based impacts. The aim of this project is to characterise Tregs located in the kidney and to expand the kidney-resident Treg population, without impacting the systemic population, in order to evaluate their specific impact on the physiology and pathologies of the kidney. First, I will characterise the kidney-resident Tregs using state-of-the-art molecular biology techniques, such as scRNAseq, and an innovative mouse model of cell fate mapping based on a photoactivatable Cre-recombinase. Second, I will evaluate their specific functions in physiology and pathologies of the kidney using a mouse model of tissue-specific Treg expansion uniquely available in the host laboratory. As well as the novel biology exploring the potential functions of kidney-resident Tregs, the distinction between systemic and kidney-based effects is critical to develop new therapeutic tools aiming to target kidney-resident Tregs. The induction of tissue-specific tolerance for kidney autoimmunity or transplantation, without inducing systemic immune suppression, constitute a promising and feasible alternative to existing immunosuppressive therapies. The knowledge and experience gained from this project combined with my scientific and personal development will give me all the skills I need to achieve my objective to pursue an exciting scientific career in academia.

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The information about "KIDNEY-TREG" are provided by the European Opendata Portal: CORDIS opendata.

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