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CD4CRISPR

A quorum sensing mechanism regulating CD4 T cell proliferation

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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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.

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

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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The information about "CD4CRISPR" are provided by the European Opendata Portal: CORDIS opendata.

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