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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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 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.

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

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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