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EXODUS SIGNED

Light induced spatially EXact and genetically encoded labeling of immune cells for monitoring of lOng Distance and Ultra-compartment Shuttling during autoimmunity and chronic inflammation

Total Cost €

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EC-Contrib. €

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Partnership

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 EXODUS project word cloud

Explore the words cloud of the EXODUS project. It provides you a very rough idea of what is the project "EXODUS" about.

cns    induction    interrogated    hypothesis    combination    travel    sclerosis    inducible    cell    vivo    window    labeling    tissue    confers    label    activated    inflammation    probe    fluorescence    cues    little    lymphoid    blue    breaking    sensed    cre    th17    compartment    resistance    translated    cells    organ    dimerizes    nervous    immunopathology    deficiency    topologically    threshold    central    tools    exodus    trace    disease    limitations    autoimmunity    immune    organs    skull    homeostasis    vice    bedrock    myeloid    body    induce    mediated    il    generation    recombinase    autoimmune    genetically    environmental    co    reverse    fundamentally    photogenetic    peripheral    split    thinned    contributed    virtually    reporter    hypotheses    ground    progeny    multiple    lag    dramatically    light    distant    surfaces    manner    epithelial    versa    anatomical    susceptibility    potency    migrate    site    sites    either    environment    physically    incidence    protein    activation    time    diseases    interfaces    licence   

Project "EXODUS" data sheet

The following table provides information about the project.

Coordinator
KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN 

Organization address
address: ISMANINGER STRASSE 22
city: MUENCHEN
postcode: 81675
website: http://www.med.tu.muenchen.de

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 Germany [DE]
 Total cost 1˙998˙063 €
 EC max contribution 1˙998˙063 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-CoG
 Funding Scheme ERC-COG
 Starting year 2015
 Duration (year-month-day) from 2015-09-01   to  2020-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN DE (MUENCHEN) coordinator 1˙998˙063.00

Map

 Project objective

The incidence of autoimmune diseases including multiple sclerosis is dramatically increasing. While there is a genetically defined “bedrock” susceptibility to develop T cell mediated autoimmunity, environmental cues likely determine the threshold for disease development. Yet, little is known on how environmental cues sensed at body/environment interfaces are translated into immunopathology in distant organs like the central nervous system (CNS). Here, we raise the hypothesis that immune cells must be activated at epithelial surfaces and then physically migrate to distant organs in order to induce autoimmunity. Furthermore, we propose that the “state of activation” of (either lymphoid or myeloid) immune cells can be interrogated by IL-6 production since IL-6 deficiency confers resistance to virtually any organ specific autoimmune disease and we have contributed fundamentally in defining the role of IL-6 for the generation of Th17 cells that are highly associated with autoimmune tissue inflammation. In EXODUS, we will develop ground-breaking next generation reporter tools in order to test these hypotheses. A split Cre recombinase protein, which dimerizes and is activated by blue light, will be used to genetically label cells (and their progeny) in a topologically defined manner (“compartment reporter”). Furthermore, we have developed a novel type of Cre-inducible in vivo IL-6 reporter (“activation reporter”). The combination of these tools will enable us to trace the anatomical compartment of activation of immune cells without limitations in lag time. Thus, site specific photogenetic co-induction of a fluorescence and IL-6 reporter will be used to probe peripheral sites for their potency to licence immune cells to travel to the CNS (Forward). Vice versa, labeling of cells in the CNS (through a thinned skull window) will allow for studying immune cell exodus from the CNS in homeostasis and during inflammation (Reverse).

 Publications

year authors and title journal last update
List of publications.
2017 Thomas Korn, Axel Kallies
T cell responses in the central nervous system
published pages: 179-194, ISSN: 1474-1733, DOI: 10.1038/nri.2016.144
Nature Reviews Immunology 17/3 2020-04-23
2016 Sylvia Heink, Nir Yogev, Christoph Garbers, Marina Herwerth, Lilian Aly, Christiane Gasperi, Veronika Husterer, Andrew L Croxford, Katja Möller-Hackbarth, Harald S Bartsch, Karl Sotlar, Stefan Krebs, Tommy Regen, Helmut Blum, Bernhard Hemmer, Thomas Misgeld, Thomas F Wunderlich, Juan Hidalgo, Mohamed Oukka, Stefan Rose-John, Marc Schmidt-Supprian, Ari Waisman, Thomas Korn
Trans-presentation of IL-6 by dendritic cells is required for the priming of pathogenic TH17 cells
published pages: 74-85, ISSN: 1529-2908, DOI: 10.1038/ni.3632
Nature Immunology 18/1 2020-04-23
2017 Andreas Muschaweckh, Franziska Petermann, Thomas Korn
IL-1β and IL-23 Promote Extrathymic Commitment of CD27 + CD122 − γδ T Cells to γδT17 Cells
published pages: 2668-2679, ISSN: 0022-1767, DOI: 10.4049/jimmunol.1700287
The Journal of Immunology 199/8 2020-04-23
2018 Christoph Garbers, Sylvia Heink, Thomas Korn, Stefan Rose-John
Interleukin-6: designing specific therapeutics for a complex cytokine
published pages: , ISSN: 1474-1776, DOI: 10.1038/nrd.2018.45
Nature Reviews Drug Discovery ePub ahead of print 2020-04-23
2017 Anna-Lena Vogel, Benjamin Knier, Katja Lammens, Sudhakar Reddy Kalluri, Tanja Kuhlmann, Jeffrey L. Bennett, Thomas Korn
Deletional tolerance prevents AQP4-directed autoimmunity in mice
published pages: 458-469, ISSN: 0014-2980, DOI: 10.1002/eji.201646855
European Journal of Immunology 47/3 2020-04-23

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