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.

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

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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