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IM-ID SIGNED

Defining the intrinsic transcriptional programs and the microenvironmental signals tailoring lung Interstitial Macrophage IDentity

Total Cost €

0

EC-Contrib. €

0

Partnership

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 IM-ID project word cloud

Explore the words cloud of the IM-ID project. It provides you a very rough idea of what is the project "IM-ID" about.

ing    dna    implicated    im    nervous    fine    little    regulators    biological    health    innovative    functions    cpg    transcription    limit    asthma    interstitial    tf    cholinergic    precise    bulk    immune    allergens    contribution    foundations    prevention    signals    recruitment    imprinted    macrophages    fundamental    underscoring    preventing    allergic    heterogeneity    date    demonstrated    dimensional    implications    niche    functional    organization    tissue    basic    elucidate    homeostasis    id    monocyte    prevent    cell    tool    protection    epithelial    chemo    instructive    function    unmethylated    single    combination    diseases    selectively    shown    expand    exposure    macrophage    aberrant    underlying    model    bacterial    signature    transgenic    dys    airway    governing    spatial    host    molecular    population    lung    differentiation    mediated    attractive    profile    programs    identity    exhibit    critical    tuning    mechanisms    precursor    technologies    tolerogenic    precursors    local    sustain   

Project "IM-ID" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE LIEGE 

Organization address
address: PLACE DU 20 AOUT 7
city: LIEGE
postcode: 4000
website: www.ulg.ac.be

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 Belgium [BE]
 Total cost 1˙500˙000 €
 EC max contribution 1˙500˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-STG
 Funding Scheme ERC-STG
 Starting year 2019
 Duration (year-month-day) from 2019-01-01   to  2023-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE LIEGE BE (LIEGE) coordinator 1˙500˙000.00

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 Project objective

The mechanisms underlying lung homeostasis are of fundamental biological importance and have critical implications for the prevention of immune-mediated diseases such as asthma. We have demonstrated that lung Interstitial Macrophages (IM) exhibit a tolerogenic profile and are able to prevent and limit the development of aberrant immune responses against allergens, thus underscoring their role as crucial regulators of lung homeostasis. In addition, we have shown that IM could expand from monocyte precursors upon host exposure to bacterial unmethylated CpG-DNA, resulting in robust protection against allergic asthma. To date, however, IM have only been characterized as a bulk population in functional studies, and little is known about the tissue-instructive signals, specific transcription factors and differentiation programs which contribute to determining their identity (ID) and function, as proposed by the macrophage niche model. We have developed an innovative transgenic tool to selectively target IM which, in combination with high dimensional single cell technologies, will allow us to (1) define the precise ID of IM, i.e. their spatial organization, heterogeneity, molecular signature and the specific TF governing their differentiation and function; (2) investigate how IM ID is imprinted by the local niche to sustain lung homeostasis. Specifically, we aim to identify the epithelial cell-derived chemo-attractive signals controlling IM precursor recruitment and to elucidate the contribution of the lung cholinergic nervous system to IM ID and lung homeostasis. This research will increase our understanding of the basic mechanisms underlying the fine-tuning of tolerogenic IM and will thus provide robust foundations for novel IM-targeted approaches promoting health and preventing airway diseases in which IM (dys)functions have been implicated.

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