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IMPACT SIGNED

Immune Mechanisms of Necrotic DNA Phagocytosis by Neutrophils: A Role for Integrins

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 IMPACT project word cloud

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

liver    beta2    recruited    chemical    internalize    amount    neutrophils    receptor    sites    day    sensing    candidates    cr3    removal    unknown    abundant    understand    billions    surprise    cell    microscopy    connected    cellular    necrosis    necrotic    existence    hypothesis    showing    cells    coated    inherently    release    body    inflammatory    lupus    phagocytose    injury    phagocytic    reports    severe    labelling    loses    express    debris    pro    erythematosus    therapies    phagocytosis    thermal    activation    diseases    death    bind    acute    integrity    thought    multicellular    models    plasma    integrins    eliminate    improper    complement    deposit    intravital    modulation    cd18    act    confocal    levels    scarce    mechanical    vitro    mediated    vivo    frequently    degrade    molecule    favor    atherosclerosis    left    promotes    membrane    peptides    remove    adhesion    combine    organisms    trauma    good    coverslip    dna    tlr9    subset    cd11b    damage    phagocytes   

Project "IMPACT" data sheet

The following table provides information about the project.

Coordinator
KATHOLIEKE UNIVERSITEIT LEUVEN 

Organization address
address: OUDE MARKT 13
city: LEUVEN
postcode: 3000
website: www.kuleuven.be

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 Belgium [BE]
 Total cost 178˙320 €
 EC max contribution 178˙320 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-01-01   to  2024-01-01

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KATHOLIEKE UNIVERSITEIT LEUVEN BE (LEUVEN) coordinator 178˙320.00

Map

 Project objective

Cell death is inherently connected to the existence of multicellular organisms. Our body loses billions of cells a day due to thermal, mechanical or chemical damage in a cell death process with loss of plasma membrane integrity and pro-inflammatory properties known as necrosis. Organisms face necrosis frequently, thus, there must be specific pathways to remove the large amount of cellular debris left behind. In this way, it is no surprise that improper removal of cellular debris, such as DNA, is associated to inflammatory diseases as lupus erythematosus, acute liver injury, atherosclerosis and severe trauma. Removal of necrotic debris is thought to be mediated by phagocytes, although reports showing it are scarce. Neutrophils, a subset of phagocytes, are good candidates for debris removal since they are abundant and quickly recruited to necrotic sites. The means used by neutrophils to identify, internalize and degrade necrotic DNA are currently unknown, thus, the main objective of my project is to understand how neutrophils phagocytose and eliminate necrotic DNA debris. Neutrophils express the DNA-sensing receptor TLR9, which is not a phagocytic receptor. However, they also express very high levels of beta2 integrins such as CD11b/CD18, which act as adhesion molecule and as complement receptor (CR3). The release of necrotic DNA promotes complement activation in vivo through several pathways, therefore, my hypothesis is that neutrophils use beta2 integrins to bind and phagocytose complement-coated necrotic DNA. To assess the role of beta2 integrins, TLR9 and complement in phagocytosis of necrotic DNA by neutrophils, I will combine a novel in vitro method (DNA deposit in coverslip) with an in vivo approach (confocal intravital microscopy). I will also develop novel peptides for DNA labelling and modulation of phagocytosis, which I will use in both models. The findings of this project will directly favor the development of novel therapies for inflammatory diseases.

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

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