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Molecular pathology of anti-viral T cell responses in the central nervous system

Total Cost €


EC-Contrib. €






Project "PATHOCODE" data sheet

The following table provides information about the project.


Organization address
city: GENEVE
postcode: 1211

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˙999˙954 €
 EC max contribution 1˙999˙954 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-05-01   to  2025-04-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE GENEVE CH (GENEVE) coordinator 1˙999˙954.00


 Project objective

'Immune responses against viruses in the central nervous system (CNS) can result in devastating outcomes. Even non-cytolytic CD8 T cell interactions, which purge viruses from neurons without triggering cell death, can induce permanent damage. Yet, how this immune response irreversibly disrupts neuronal homeostasis remains unclear. Here, we will elucidate the molecular mechanisms that underlie non-cytolytic CD8 T cell engagement with infected neurons and their consequences on neuron function in vivo. We hypothesize that inflammatory signalling in neurons, induced by non-cytolytic CD8 T cell interactions, triggers metabolic and epigenetic changes that underpin permanent neuronal dysfunction. 'PATHOCODE' will test this hypothesis by harnessing a unique animal model of T cell-driven virus encephalitis in the following objectives: 1. Discern neuronal subset-specific vulnerabilities and antigen-dependent versus bystander effects in the inflamed CNS. We will perform single nucleus RNA sequencing to examine whether T cell engagement (a) differentially affects molecularly distinct neurons, and (b) affects non-targeted, uninfected neurons. 2. Uncover the consequences of non-cytolytic T cell engagement on neuronal metabolism. We will use cell-specific mitochondrial reporter mice to investigate immune-driven metabolic adaptation of neurons in vivo. 3. Determine how non-cytolytic T cell engagement affects the neuronal epigenome. We will employ cell-specific nucleus/ribosome reporter mice to elucidate how T cell engagement affects the translatome and epigenome of infected cells. 4. Rescue T cell-mediated neuronal dysfunction by restoring metabolic pathways. We will exploit recent CRISPR/Cas9 technological advances to restore neuronal gene expression and uncover the relevance of immune-driven metabolic and epigenomic changes to disease. Our study will thus provide novel molecular concepts about immune-driven neuronal alterations in CNS inflammatory diseases.'

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

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