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Signalling-in-NODs

Investigation of the role and mechanism of action of NOD2-mediated isoform selective PI3K signalling in gut immunity and inflammation

Total Cost €

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EC-Contrib. €

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Partnership

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 Signalling-in-NODs project word cloud

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

pathogen    ibd    integrate    tolerance    made    receptor    animal    immune    oligomerization    prr    p110    action    variants    gene    linked    kinases    susceptibility    immunity    conserved    pathology    models    functions    molecular    genetic    mutations    alongside    roles    little    inflammation    phenomena    components    vivo    chronic    dysregulated    innate    biology    either    proteins    autophagy    messengers    pharmacological    unravel    societies    nod    mice    orchestrating    recognition    immunology    isoforms    underlying    risk    gut    anti    protective    signaling    nod2    discover    cell    strategies    driving    single    discovered    pi3ks    evolutionarily    unmet    dendritic    initiated    generate    microbial    deleterious    elucidate    lipid    bowel    inflammatory    molecules    intrinsic    nucleotide    domain    phosphoinositide    intestinal    host    mechanisms    caused    mediated    peptides    plan    biological    disease    convey    regulate    nlr    isoform    despite    family    delta    therapeutic    pi3k    mechanism    microbiology    protection    regulating    programs    phenomenon    western   

Project "Signalling-in-NODs" 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 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-05-01   to  2019-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    QUEEN MARY UNIVERSITY OF LONDON UK (LONDON) coordinator 195˙454.00

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 Project objective

Inflammatory bowel disease (IBD) is a complex chronic pathology in western societies. There is an unmet need for new therapeutic strategies which can only be achieved through a better understanding of the molecular mechanisms of host immunity. It is established that dysregulated host innate immune recognition either caused by genetic risk variants in pathogen recognition receptor (PRR) molecules or microbial factors is commonly associated with IBD. A unique PRR family member, Nucleotide oligomerization domain (NOD)2 programs gut immunity and protection through autophagy process initiated by the recognition of microbial peptides. Deleterious mutations in NOD2 and autophagy-associated proteins are linked to IBD susceptibility. Despite the advances made in understanding of the mechanisms underlying NOD2 biology, particularly that of autophagy, very little is known about the cell signaling components and their mechanism regulating autophagy under NOD2 pathway. Recently, I discovered that a single Phosphoinositide 3-kinases (PI3K) isoform p110δ is integrated in NOD2 mediated autophagy process. PI3Ks are an evolutionarily conserved family of signaling molecules that integrate PRR signaling. PI3Ks generate lipid second messengers and regulate mediated immune responses. I now propose to unravel key biological phenomenon by which p110δ PI3K convey host protective functions through NOD2-mediated autophagy, ensuring the gut immunity and tolerance. The aims are to (1) Determine the dendritic cell-intrinsic role and mechanism(s) of action of PI3K isoforms in orchestrating anti-inflammatory processes under NOD2-mediated autophagy. (2) Discover the roles of PI3K isoforms in NLR-mediated intestinal immunity using isoform specific PI3K gene-targeted mice alongside with pharmacological targeting strategies in vivo. My plan is integrated with animal models, immunology, cell biology, microbiology and in vivo inflammation studies to elucidate key biological phenomena driving IBD.

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