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MitoGuide SIGNED

Integration and adaptation of impaired mitochondrial fitness in orchestrating T cell dysfunction in the tumor microenvironment

Total Cost €

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EC-Contrib. €

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Partnership

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Project "MitoGuide" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE LAUSANNE 

Organization address
address: Quartier Unil-Centre Bâtiment Unicentre
city: LAUSANNE
postcode: 1015
website: www.unil.ch

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 Switzerland [CH]
 Total cost 1˙499˙990 €
 EC max contribution 1˙499˙990 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-STG
 Funding Scheme ERC-STG
 Starting year 2019
 Duration (year-month-day) from 2019-02-01   to  2024-01-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE LAUSANNE CH (LAUSANNE) coordinator 1˙499˙990.00

Map

 Project objective

Cancer immunotherapies harnessing the tumoricidal activity of tumor-reactive T cells represent a major breakthrough in the current paradigm for treating cancer patents. However, the highly immunosuppressive tumor microenvironments found in solid tumors present challenges by restricting the tumoricidal functions and metabolic fitness of infiltrating tumor-reactive T cells. Given that the activation-induced metabolic switch is tightly intertwined with T cell activities, restoring the metabolic fitness of T cells represents a promising strategy for strengthening anti-tumor immunity. However, the success of this strategy relies on our understanding of the underlying mechanisms utilized by tumor cells to abolish the metabolic fitness of T cells, and of how metabolic programming controls T cell functions. Based on our preliminary results, we postulate that tumor cells disrupt the mitochondrial dynamics of tumor-infiltrating T cells by interrupting mitophagy. This causes a metabolic crisis for the infiltrating T cells in sustaining their metabolic fitness and flexibility. Furthermore, we hypothesize that declined mitochondria-derived retrograde signals resulted from mitochondrial dysfunction may lead to T cell dysfunction/exhaustion and altered immune responses through epigenetic reprogramming and altered proteome-metabolic regulatory circuits. The objectives of this proposal are to delineate how tumor cells influence the mitochondrial dynamics of T cells and define the unexplored immunometabolic regulations of T cell functions that are controlled by mitochondria. Lastly, we aim to new methods to restore missing retrograde signals in T cells, which could allow them to prevent mitochondrial dysfunction-induced epigenetic and transcriptomic changes. This work represents an entirely new perspective on control of T cell functions by the immunosuppressive tumor microenvironment, and it may reveal new dimensions of immunometabolic regulation.

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The information about "MITOGUIDE" are provided by the European Opendata Portal: CORDIS opendata.

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