Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

Kerstin Göbel (), Susann Pankratz, Chloi-Magdalini Asaridou, Alexander M. Herrmann, Stefan Bittner, Monika Merker, Tobias Ruck, Sarah Glumm, Friederike Langhauser, Peter Kraft, Thorsten F. Krug, Johanna Breuer, Martin Herold, Catharina C. Gross, Denise Beckmann, Adelheid Korb-Pap, Michael K. Schuhmann, Stefanie Kuerten, Ioannis Mitroulis, Clemens Ruppert, Marc W. Nolte, Con Panousis, Luisa Klotz, Beate Kehrel, Thomas Korn, Harald F. Langer, Thomas Pap, Bernhard Nieswandt, Heinz Wiendl, Triantafyllos Chavakis, Christoph Kleinschnitz and Sven G. Meuth ()
Additional contact information
Kerstin Göbel: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Susann Pankratz: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Chloi-Magdalini Asaridou: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Alexander M. Herrmann: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Stefan Bittner: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Monika Merker: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Tobias Ruck: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Sarah Glumm: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Friederike Langhauser: University Hospital Würzburg
Peter Kraft: University Hospital Würzburg
Thorsten F. Krug: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Johanna Breuer: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Martin Herold: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Catharina C. Gross: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Denise Beckmann: Institute of Experimental Musculoskeletal Medicine, University Hospital Münster
Adelheid Korb-Pap: Institute of Experimental Musculoskeletal Medicine, University Hospital Münster
Michael K. Schuhmann: University Hospital Würzburg
Stefanie Kuerten: University of Würzburg
Ioannis Mitroulis: University Clinic Carl Gustav Carus, Technische Universität of Dresden
Clemens Ruppert: Universities of Giessen & Marburg Lung Center (UGMLC)/Member of the German Center for Lung Research (DZL), Justus-Liebig University
Marc W. Nolte: CSL Behring GmbH
Con Panousis: CSL Limited, Bio21 Institute
Luisa Klotz: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Beate Kehrel: Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster
Thomas Korn: Klinikum rechts der Isar, Technical University of Munich
Harald F. Langer: Section for Cardioimmunology, University Clinic of Tübingen
Thomas Pap: Institute of Experimental Musculoskeletal Medicine, University Hospital Münster
Bernhard Nieswandt: Rudolf Virchow Center, Deutsche Forschungsgemeinschaft Research Center for Experimental Biomedicine, University of Würzburg
Heinz Wiendl: Clinic of Neurology and Institute for Translational Neurology, University of Münster
Triantafyllos Chavakis: University Clinic Carl Gustav Carus, Technische Universität of Dresden
Christoph Kleinschnitz: University Hospital Würzburg
Sven G. Meuth: Clinic of Neurology and Institute for Translational Neurology, University of Münster

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: Abstract Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells. Immune activation by FXII is mediated by dendritic cells in a CD87-dependent manner and involves alterations in intracellular cyclic AMP formation. Our study demonstrates that a member of the plasmatic coagulation cascade is a key mediator of autoimmunity. FXII inhibition may provide a strategy to combat MS and other immune-related disorders.

Date: 2016
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DOI: 10.1038/ncomms11626

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