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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.

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

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

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