Opendata, web and dolomites


Sorting of Self

Total Cost €


EC-Contrib. €






 SOS project word cloud

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

identification    data    comprehensively    track    elucidate    inflammation    incorrect    permanently    mapping    simultaneous    remained    transgenic    conjunction    elusive    ac    cre    autoimmunity    necrotic    apoptotic    mechanisms    sorting    endogenously    sorts    vivo    initiation    thereby    insights    immune    dying    incompletely    tat    therapeutic    animals    macrophages    diseases    respectively    strategies    form    immunogenic    fate    infectious    break    generate    confronted    follow    plan    inflammatory    pro    disorders    simultaneously    technologies    segregated    infection    self    differentiation    during    cells    reporter    molecular    accumulated    mice    acs    ingestion    aberrant    phagocytes    treatment    antigens    antigen    laboratory    presenting    tolerance    autoimmune    subsequent    underlying    pathogenesis    limitations    largely    eyfp    entities    clearance    bacteria    subspecies    tools    dendritic    parallel    r26    pathogens    mediate    cutting    invading    actively    phagocyte    migratory    edge    differential    microbes   

Project "SOS" data sheet

The following table provides information about the project.


Organization address
postcode: 91054

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]
 Project website
 Total cost 1˙479˙781 €
 EC max contribution 1˙479˙781 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-STG
 Funding Scheme ERC-STG
 Starting year 2015
 Duration (year-month-day) from 2015-05-01   to  2020-04-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

During inflammation and infection, we are simultaneously confronted with both self and non-self in form of dying cells and microbes, respectively. Mechanisms that facilitate the non-immunogenic clearance of self-antigens derived from apoptotic and necrotic cells and that, in parallel, allow the initiation of an immune response against invading pathogens are incompletely understood. Recent data from our laboratory show that the immune system actively sorts apoptotic cells (ACs) and bacteria into distinct subspecies of macrophages and dendritic cells thereby enabling a segregated processing of self and non-self as well as a differential immune response against these two entities. Incorrect sorting and aberrant uptake of AC-derived self-antigens by pro-inflammatory and antigen-presenting dendritic cells, however, results in the break of self-tolerance and autoimmunity. Due to technical limitations, the identification and fate-mapping of specific phagocyte subsets that mediate the simultaneous clearance of dying cells and pathogens in vivo has remained largely elusive. We thus plan to develop novel tools that are based on cutting-edge technologies to comprehensively elucidate the sorting of dying cells and pathogens under inflammatory conditions in vivo. We plan to generate TAT-Cre transgenic mice and bacteria that will be used in conjunction with R26-eYFP reporter animals to permanently track phagocytes after ingestion of endogenously accumulated dying cells and pathogens, respectively. These approaches will enable us to characterize the involved phagocytes, study molecular mechanisms underlying the differential processing of self and non-self and follow the phagocyte’s migratory behaviour and its subsequent differentiation. The obtained data will not only provide insights into the pathogenesis of autoimmune and infectious diseases, but will also foster the development of novel therapeutic strategies for the treatment of such disorders.


year authors and title journal last update
List of publications.
2017 Tobias Rothe, Natacha Ipseiz, Maria Faas, Stefanie Lang, Francesc Perez-Branguli, Daniel Metzger, Hiroshi Ichinose, Beate Winner, Georg Schett, Gerhard Krönke
The Nuclear Receptor Nr4a1 Acts as a Microglia Rheostat and Serves as a Therapeutic Target in Autoimmune-Driven Central Nervous System Inflammation
published pages: 3878-3885, ISSN: 0022-1767, DOI: 10.4049/jimmunol.1600638
The Journal of Immunology 198/10 2019-05-29
2016 René Pfeifle, Tobias Rothe, Natacha Ipseiz, Hans U Scherer, Stephan Culemann, Ulrike Harre, Jochen A Ackermann, Martina Seefried, Arnd Kleyer, Stefan Uderhardt, Benjamin Haugg, Axel J Hueber, Patrick Daum, Gordon F Heidkamp, Changrong Ge, Sybille Böhm, Anja Lux, Wolfgang Schuh, Iryna Magorivska, Kutty S Nandakumar, Erik Lönnblom, Christoph Becker, Diana Dudziak, Manfred Wuhrer, Yoann Rombouts, Carolien A Koeleman, René Toes, Thomas H Winkler, Rikard Holmdahl, Martin Herrmann, Stephan Blüml, Falk Nimmerjahn, Georg Schett, Gerhard Krönke
Regulation of autoantibody activity by the IL-23–TH17 axis determines the onset of autoimmune disease
published pages: , ISSN: 1529-2908, DOI: 10.1038/ni.3579
Nature Immunology 2019-05-29

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The information about "SOS" are provided by the European Opendata Portal: CORDIS opendata.

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