Monoclonal and oligoclonal anti-platelet factor 4 antibodies mediate VITT

Author:

Kanack Adam J.1,Bayas Antonios2,George Gemlyn3,Abou-Ismail Mouhamed Yazan4ORCID,Singh Bandana1,Kohlhagen Mindy C.1,Splinter Noah P.1,Christ Monika2,Naumann Markus2,Moser Karen A.56,Smock Kristi J.56ORCID,Grazioli Alison78,Wen Renren9ORCID,Wang Demin9,Murray David L.1,Padmanabhan Anand1ORCID

Affiliation:

1. 1Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN;

2. 2Department of Neurology and Clinical Neurophysiology, University Hospital of Augsburg, Augsburg, Germany;

3. 3Department of Medicine, University of Colorado, Aurora, CO;

4. 4Department of Medicine and

5. 5Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, UT;

6. 6ARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT;

7. 7National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD;

8. 8Division of Pulmonary and Critical Care Medicine, University of Maryland School of Medicine, Baltimore, MD; and

9. 9Blood Research Institute, Versiti, Milwaukee, WI

Abstract

Kanack and colleagues analyze anti-platelet factor 4 antibodies from 5 patients with vaccine-induced thrombotic thrombocytopenia (VITT) secondary to COVID-19 adenoviral vaccination and antibodies from patients with spontaneous heparin-induced thrombocytopenia (HIT) and classical HIT. VITT antibodies are monoclonal or oligoclonal, similar to spontaneous HIT, whereas classical HIT antibodies are polyclonal. Heparin inhibits antibody-induced platelet activation in VITT, suggesting that heparin should be considered for the treatment of VITT.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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