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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.

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

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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