Nature Communications (Feb 2018)
A ligand-specific blockade of the integrin Mac-1 selectively targets pathologic inflammation while maintaining protective host-defense
- Dennis Wolf,
- Nathaly Anto-Michel,
- Hermann Blankenbach,
- Ansgar Wiedemann,
- Konrad Buscher,
- Jan David Hohmann,
- Bock Lim,
- Marina Bäuml,
- Alex Marki,
- Maximilian Mauler,
- Daniel Duerschmied,
- Zhichao Fan,
- Holger Winkels,
- Daniel Sidler,
- Philipp Diehl,
- Dirk M Zajonc,
- Ingo Hilgendorf,
- Peter Stachon,
- Timoteo Marchini,
- Florian Willecke,
- Maximilian Schell,
- Björn Sommer,
- Constantin von zur Muhlen,
- Jochen Reinöhl,
- Teresa Gerhardt,
- Edward F. Plow,
- Valentin Yakubenko,
- Peter Libby,
- Christoph Bode,
- Klaus Ley,
- Karlheinz Peter,
- Andreas Zirlik
Affiliations
- Dennis Wolf
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Nathaly Anto-Michel
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Hermann Blankenbach
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Ansgar Wiedemann
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Konrad Buscher
- Inflammation Biology, La Jolla Institute for Allergy and Immunology
- Jan David Hohmann
- Atherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute
- Bock Lim
- Atherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute
- Marina Bäuml
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Alex Marki
- Inflammation Biology, La Jolla Institute for Allergy and Immunology
- Maximilian Mauler
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Daniel Duerschmied
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Zhichao Fan
- Inflammation Biology, La Jolla Institute for Allergy and Immunology
- Holger Winkels
- Inflammation Biology, La Jolla Institute for Allergy and Immunology
- Daniel Sidler
- Division of Nephrology, Inselspital, Bern University Hospital
- Philipp Diehl
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Dirk M Zajonc
- Division of Cell Biology, La Jolla Institute for Allergy and Immunology
- Ingo Hilgendorf
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Peter Stachon
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Timoteo Marchini
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Florian Willecke
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Maximilian Schell
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Björn Sommer
- Neurosurgery, Medical Faculty of the University of Erlangen
- Constantin von zur Muhlen
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Jochen Reinöhl
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Teresa Gerhardt
- Inflammation Biology, La Jolla Institute for Allergy and Immunology
- Edward F. Plow
- Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic
- Valentin Yakubenko
- Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic
- Peter Libby
- Brigham and Women’s Hospital, Cardiovascular Medicine, Harvard Medical School
- Christoph Bode
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- Klaus Ley
- Inflammation Biology, La Jolla Institute for Allergy and Immunology
- Karlheinz Peter
- Atherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute
- Andreas Zirlik
- Cardiology and Angiology I, University Heart Center, and Medical Faculty, University of Freiburg
- DOI
- https://doi.org/10.1038/s41467-018-02896-8
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 11
Abstract
Integrin-based therapeutics could block inflammatory processes but they also impair host defence, limiting their usefulness. Here the authors report an anti-Mac1 antibody that blocks its interaction with pro-inflammatory ligand CD40L but not other ligands, and show that it can protect against sepsis in mice.
