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MIMIC SIGNED

Deciphering how microbiota modulate anti-tumor immune responses in checkpoint therapy

Total Cost €

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EC-Contrib. €

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Partnership

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Project "MIMIC" data sheet

The following table provides information about the project.

Coordinator
INSTITUT CURIE 

Organization address
address: rue d'Ulm 26
city: PARIS
postcode: 75231
website: www.curie.fr

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 France [FR]
 Total cost 184˙707 €
 EC max contribution 184˙707 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2022-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT CURIE FR (PARIS) coordinator 184˙707.00

Map

 Project objective

Microbiota has a major impact on anti-tumor immune responses and efficacy of anticancer treatments. These effects are thought to be mediated by modulation of tumor-infiltrating myeloid cells. These include immunosuppressive macrophages that differentiate from inflammatory monocytes recruited to the tumor. However, what microbiota-derived products are required for efficient anti-tumoral responses is still unclear. We have recently identified the Aryl Hydrocarbon Receptor (AhR) as a key suppressor of monocyte-to-macrophage differentiation. AhR is a ligand-activated transcription factor sensing metabolites derived mainly from dietary intake and microbiota metabolism. Based on our previous work, we hypothesize that AhR is involved in the modulation of anti-tumoral responses by the microbiota, via the regulation of immune cells differentiation or function. The objective of the project is to address whether AhR ligands mediate the impact of microbiota on anti-tumor responses in anti-checkpoint therapy and to determine the cellular mechanisms involved. To address it, we will analyse anti-tumor immune responses in groups of mice with normal or altered microbiota, treated or not with anticheckpoint therapy, fed with a control diet or supplemented for AhR ligands. We will combine two complimentary approaches, employing antibiotics to deplete the microbiota or using germfree mice. The efficacy of immunotherapies using checkpoint inhibitors is greatly reduced in patients who receive antibiotics. This is a major issue as antibiotics are commonly prescribed to prevent or treat infections in cancer patients, who may be vulnerable. This research project will provide critical novel insight into the complex interplay between microbiota and anti-tumor immune responses. Results from this project will be instrumental in designing novel strategies for improving anti-tumoral immunotherapies.

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