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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.

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

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

Map

 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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