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PI3K-in-tolerance SIGNED

PI3K delta role in dendritic cell antigen processing and presentation to control gut tolerance

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EC-Contrib. €

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 PI3K-in-tolerance project word cloud

Explore the words cloud of the PI3K-in-tolerance project. It provides you a very rough idea of what is the project "PI3K-in-tolerance" about.

mediating    shows    genes    recognition    pathogen    induce    pi3k    model    prrs    muramyl    activated    triggered    homeostasis    originating    cgd    shown    app    pi3ks    dcs    animal    phagosome    dc    opportunistic    presented    bacteriodes    fragilis    vesicular    dipeptide    innate    activation    linked    resistance    pathogens    il10    vesicles    antigens    preliminary    interactions    senses    trafficking    presentation    delta    microbiota    granulomatous    domain    environmental    inducing    functions    cd    treg    encoding    vitro    nadph    dysregulated    patients    microbiome    spontaneously    kinase    susceptibility    chronic    receptors    oxidase    mhcii    maintaining    ros    cd4    inactivated    immunity    crohn    concurrently    colitis    gtpase    gut    intestinal    activate    family    rac2    signalling    commensal    species    prr    cell    events    mechanisms    pathology    mutations    first    tolerance    disease    data    documented    defects    released    nox2    oxygen    stimulate    controls    nod2    omvs    subunits    phagosomal    intrinsic    antigen    sites    bridge    biological    reactive    gene    bacteria    membrane    critical    adaptive    outer    mice    engagement    mucosal    signaling    tregs   

Project "PI3K-in-tolerance" data sheet

The following table provides information about the project.

Coordinator
QUEEN MARY UNIVERSITY OF LONDON 

Organization address
address: 327 MILE END ROAD
city: LONDON
postcode: E1 4NS
website: http://www.qmul.ac.uk

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 United Kingdom [UK]
 Total cost 212˙933 €
 EC max contribution 212˙933 € (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 2019
 Duration (year-month-day) from 2019-09-01   to  2021-08-31

 Partnership

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# participants  country  role  EC contrib. [€] 
1    QUEEN MARY UNIVERSITY OF LONDON UK (LONDON) coordinator 212˙933.00

Map

 Project objective

PI3Ks controls important biological processes immunity controlling vesicular trafficking and cell signaling events triggered by pathogen recognition receptors (PRRs). The engagement of PRRs leading to DC antigen processing and presentation (APP) is essential for the bridge between innate and adaptive immunity. Thus, DCs are crucial for resistance against pathogens, while concurrently maintaining tolerance to the commensal microbiota and environmental antigens. Crohn’s disease (CD)-like pathology has been documented in patients with chronic granulomatous disease (CGD), originating from mutations in genes encoding NADPH oxidase (NOX2) subunits or RAC2 GTPase. Both PRR-activated NOX2 and RAC2 are critical for inducing phagosomal reactive oxygen species (ROS) linked to APP processes in the DC. Thus, that dysregulated PRR signalling and NOX2 activity in the DC phagosome, may be key steps involved in some of the pathology observed in CD. The PRR family member NOD2 senses muramyl dipeptide in bacteria. NOD2 was the first susceptibility gene identified for CD and associated with tolerance mechanisms mediating intestinal homeostasis to gut microbiota. Recently, interactions between NOD2 and microbiome were shown to stimulate Treg activity at the mucosal sites. Bacteria-derived outer membrane vesicles (OMVs) from gut commensal Bacteriodes fragilis induce mucosal tolerance by DC-intrinsic activation of NOD2 and enabling DCs to induce IL10 production from Tregs. It is known that OMVs require NOX2-induced ROS to be released for APP and presented by MHCII to activate CD4 Tregs. Our preliminary data shows that mice inactivated in the kinase domain of PI3K delta spontaneously develop colitis in the presence of an intestinal opportunistic pathogens and show defects in antigen presentation in DCs in vitro. Based on these results, I propose to investigate the DC-intrinsic PI3K role in APP functions that control gut tolerance in this animal model of colitis.

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