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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.

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

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

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 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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