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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.

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

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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