Explore the words cloud of the BASILIC project. It provides you a very rough idea of what is the project "BASILIC" about.
The following table provides information about the project.
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS
|Coordinator Country||France [FR]|
|Total cost||2˙000˙000 €|
|EC max contribution||2˙000˙000 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2018-08-01 to 2022-07-31|
Take a look of project's partnership.
|1||CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS||FR (PARIS)||coordinator||2˙000˙000.00|
Although the T cell antigen receptor (TCR) occupies a central place in T cell physiology, it does not work in isolation and the signals it triggers are tuned by receptors that convey positive (costimulators) and negative (coinhibitors) informations. We lack a satisfying comprehension of the way T cells integrate such multiple inputs to make informed decisions. The proteomics-based methodology we developed around the TCR places us in a favorable situation to decode at systems-level the crosstalk between the TCR, the CD28 costimulator and the PD-1 coinhibitor signaling pathways. The novelty of our approach stems from (1) its use of primary T cells, (2) its capacity to probe the architecture and dynamics of signalosomes resulting from T cell-antigen presenting cell encounters, (3) the attention we pay to the stoichiometry of the studied signalosomes, a key parameter largely ignored in previous studies, and (4) its multidisciplinary nature straddling molecular and organismal scales. Our specific aims are: Aim 1. To understand how the TCR and CD28 signaling pathways cooperate to achieve optimal T cell responses. Aim 2. To determine whether CD28 is the sole target of the PD-1 coinhibitor. Aim 3. To determine how under inflammatory conditions CD28 functions can be superseded by those of OX40, a costimulator of the TNFR superfamily. Aim 4. To unveil how malfunctions of LAT, a key signaling hub used by the TCR, disrupt the TCR-CD28 crosstalk and result in unique pathogenic T cells that by becoming ‘autistic’ to TCR signals and addicted to CD28 signals lead to severe immunopathologies. We think that combining genetic, epigenomics, proteomics, and computational approaches creates ideal experimental conditions to understand at system-levels how TCR, costimulatory, coinhibitory and inflammatory signals are integrated during T cell clonal expansion. Although of fundamental nature, our project should help understanding the harmful role PD-1 plays during anti-tumoral responses.
|year||authors and title||journal||last update|
Guillaume Voisinne, Kristof Kersse, Karima Chaoui, Liaoxun Lu, Julie Chaix, Lichen Zhang, Marisa Goncalves Menoita, Laura Girard, Youcef Ounoughene, Hui Wang, Odile Burlet-Schiltz, HervÃ© Luche, FrÃ©dÃ©ric Fiore, Marie Malissen, Anne Gonzalez de Peredo, Yinming Liang, Romain Roncagalli, Bernard Malissen
Quantitative interactomics in primary T cells unveils TCR signal diversification extent and dynamics
published pages: 1530-1541, ISSN: 1529-2908, DOI: 10.1038/s41590-019-0489-8
|Nature Immunology 20/11||2020-04-24|
Javier Celis-Gutierrez, Peter Blattmann, Yunhao Zhai, Nicolas Jarmuzynski, Kilian Ruminski, Claude GrÃ©goire, Youcef Ounoughene, FrÃ©dÃ©ric Fiore, Ruedi Aebersold, Romain Roncagalli, Matthias Gstaiger, Bernard Malissen
Quantitative Interactomics in Primary T Cells Provides a Rationale for Concomitant PD-1 and BTLA Coinhibitor Blockade in Cancer Immunotherapy
published pages: 3315-3330.e7, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2019.05.041
|Cell Reports 27/11||2019-09-05|
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