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

Author

Listed:
  • 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
    University Medical Center of the Johannes Gutenberg-University)

  • 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
    University Hospital Essen)

  • Sven G. Meuth

    (Clinic of Neurology and Institute for Translational Neurology, University of Münster)

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.

Suggested Citation

  • 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, 2016. "Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells," Nature Communications, Nature, vol. 7(1), pages 1-16, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11626
    DOI: 10.1038/ncomms11626
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    Cited by:

    1. Pengfei Xu & Yingjie Zhang & Junyan Guo & Huihui Li & Sandra Konrath & Peng Zhou & Liming Cai & Haojie Rao & Hong Chen & Jian Lin & Zhao Cui & Bingyang Ji & Jianwei Wang & Nailin Li & De-Pei Liu & Tho, 2024. "A single-domain antibody targeting factor XII inhibits both thrombosis and inflammation," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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