Amplification of bacteria-induced platelet activation is triggered by FcγRIIA, integrin αIIbβ3, and platelet factor 4

Author:

Arman Mònica1,Krauel Krystin23,Tilley Dorothea O.4,Weber Claudia5,Cox Dermot4,Greinacher Andreas2,Kerrigan Steven W.4,Watson Steve P.1

Affiliation:

1. Centre for Cardiovascular Sciences, Institute of Biomedical Research, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom;

2. Institut für Immunologie und Transfusionsmedizin, Universitätsmedizin Greifswald, Greifswald, Germany;

3. Zentrum für Innovationskompetenz–Humorale Immunreaktionen bei Kardiovaskulären Erkrankungen, Universitätsmedizin Greifswald, Greifswald, Germany;

4. Cardiovascular Infection Group, Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland; and

5. Abteilung Genetik der Mikroorganismen, Interfakultäres Institut für Genetik und Funktionelle Genomforschung, Ernst-Moritz-Arndt-Universität Greifswald, Greifswald, Germany

Abstract

Key Points FcγRIIA activation is key for platelet aggregation in response to bacteria, and depends on IgG and αIIbβ3 engagement. PF4 binds to bacteria and reduces the lag time for platelet aggregation.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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