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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.

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

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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