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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.

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

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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