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Pathogen Oriented SNARE Trafficking for Immune Tailoring

Total Cost €


EC-Contrib. €






 POST-IT project word cloud

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

quantitative    presentation    harmless    proteins    recognition    pathogen    imaging    resolve    immune    fret    disease    minority    antigen    adaptive    binding    snare    roles    data    clearance    flim    trafficking    resonance    trigger    healthy    ingest    lacking    toll    microscopy    dcs    fusion    altered    bio    energy    triggers    ingested    histocompatibility    diseases    chemistry    alters    complexes    signaling    receptor    lifetime    self    transporters    mediated    receptors    vaccinations    mhc    rster    ouml    cells    activation    correct    prevent    phosphorylation    promoted    recruitment    autonomous    promotes    oriented    fluorescence    antigens    phagosomal    macrophages    functional    phagosome    membrane    molecular    infectious    literature    proteases    phagosomes    technique    dendritic    preliminary    therapies    pathogens    multiple    peptides    function    orthogonal    snares    hypothesize    transfer    imimmune    cell    sensitivity    autoimmune    turn   

Project "POST-IT" data sheet

The following table provides information about the project.


Organization address
address: Broerstraat 5
postcode: 9712CP

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 Netherlands [NL]
 Total cost 2˙000˙000 €
 EC max contribution 2˙000˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-05-01   to  2025-04-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

ImImmune clearance of infectious diseases requires correct T cell activation by macrophages and dendritic cells (DCs) that present peptides derived from ingested pathogens on major histocompatibility complexes (MHC). Yet, macrophages and DCs also ingest self-antigens present in healthy cells and their presentation might trigger autoimmune disease. Presentation of the minority of ingested pathogens is promoted by so-called phagosome-autonomous trafficking. Here, pathogen binding to Toll-like receptors in phagosomes triggers recruitment of proteases and transporters to these phagosomes, but not to other phagosomes present in the same cell, promoting specific presentation of pathogen-derived peptides. However, a molecular understanding of this pathogen-oriented phagosome-autonomous trafficking is lacking. The goal of this project is to determine how phagosome-autonomous pathogen recognition promotes presentation of pathogen-derived over harmless self-antigens. Based on my preliminary data and literature, I hypothesize that Toll-like receptor signaling triggers phosphorylation of multiple SNARE proteins at the phagosomal membrane. As SNARE phosphorylation can promote or prevent membrane fusion, this alters delivery of proteases and transporters to these phagosomes, which in turn promotes presentation of pathogen-derived peptides. Objective 1 is to determine how SNARE function is altered upon pathogen-recognition in phagosomes using my novel quantitative Förster resonance energy transfer-fluorescence lifetime imaging microscopy (FRET-FLIM)-based technique. Objective 2 is to address how Toll-like receptor-mediated SNARE phosphorylation affects phagosome-autonomous trafficking. Objective 3 is to resolve the functional roles of SNAREs in antigen presentation using a novel bio-orthogonal chemistry-based method. This study will explain the high sensitivity of the adaptive immune system for pathogens and could lead to better vaccinations and therapies for infectious diseases.

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The information about "POST-IT" are provided by the European Opendata Portal: CORDIS opendata.

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