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CD4CRISPR

A quorum sensing mechanism regulating CD4 T cell proliferation

Total Cost €

0

EC-Contrib. €

0

Partnership

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 CD4CRISPR project word cloud

Explore the words cloud of the CD4CRISPR project. It provides you a very rough idea of what is the project "CD4CRISPR" about.

populations    regulate    efficacy    efficient    extensively    tgf    expressing    limits    generate    intrinsic    feedback    direct    vivo    molecularly    priming    optimization    interfere    disorders    inducible    strategy    rag    first    migration    loop    productive    mouse    demonstrated    reactive    documented    infection    genes    proliferative    ag    named    proof    regulation    inactivate    dampen    exclusion    capacity    constitutive    cas9    mechanisms    autoimmune    gamma    inflammatory    enriched    sgrna    memory       resolution    pd    coupled    mice    effector    tcr    receptor    transgenic    ifn    knockout    cd4    mechanism    strain    preferential    candidate    cells    fine    immune    marilyn    cohort    negative    antigen    antitumor    signals    immunized    primary    cancer    screen    dby    orchestrating    viral    proliferation    regulators    expansion    genome    suppressive    l1    cell    therapeutic    ongoing    library    diseases    vaccine    contraction    interactions    immunotherapy   

Project "CD4CRISPR" data sheet

The following table provides information about the project.

Coordinator
INSTITUT CURIE 

Organization address
address: rue d'Ulm 26
city: PARIS
postcode: 75231
website: www.curie.fr

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 France [FR]
 Project website https://science.curie.fr/recherche/biologie-interactive-des-tumeurs-immunologie-environnement/immunite-et-cancer/equipe-lantz/
 Total cost 185˙076 €
 EC max contribution 185˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-04-01   to  2019-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT CURIE FR (PARIS) coordinator 185˙076.00

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 Project objective

The fine and complex regulation of CD4 immune response is important in cancer, autoimmune diseases, inflammatory disorders and viral infection. If signals orchestrating productive CD4 T-cell responses are well documented, the contraction of antigen (Ag)-specific CD4 T-cell populations following the resolution of primary immune response is however not molecularly understood. It has been demonstrated that a negative feedback loop can regulate CD4 T cell proliferation through direct T-T interactions, leading to the preferential exclusion of Ag-experienced T cells. This T cell intrinsic mechanism limits the expansion of effector CD4 T cells and may then interfere with therapeutic vaccine efficacy. Using Cas9-(constitutive/inducible)-expressing Dby-reactive T cells (from a TCR Transgenic RAG-/- mouse strain named Marilyn) coupled to a sgRNA library and an in vivo selection strategy, we will extensively identify the negative regulators of CD4 T cells migration and priming in an ongoing primary immune response. As a proof of concept, we will first inactivate candidate genes (already known to be involved in CD4 T cells negative regulation: TGF-b receptor,IFN-γ receptor, PD-1 and PD-L1) in Ag-experienced memory CD4 T cells, which will be enriched for their proliferative capacity in vivo and used as a second cohort in immunized mice. Then, we will develop a genome-wide screen approach to generate a library of knockout Ag-experienced T cells as a second cohort. We expect that further insight into CD4 suppressive mechanisms, which dampen efficient antitumor immune responses, will allow optimization of cancer immunotherapy.

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