Heparin-independent, PF4-dependent binding of HIT antibodies to platelets: implications for HIT pathogenesis-Reference-Cited by-同舟云学术

Heparin-independent, PF4-dependent binding of HIT antibodies to platelets: implications for HIT pathogenesis

Published:2015-01-01 Issue:1 Volume:125 Page:155-161
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Padmanabhan Anand¹²³,Jones Curtis G.¹,Bougie Daniel W.²,Curtis Brian R.²⁴,McFarland Janice G.⁴⁵,Wang Demin²⁶,Aster Richard H.²⁵

Affiliation:

1. Medical Sciences Institute and

2. Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI;

3. Department of Pathology, Medical College of Wisconsin, Milwaukee, WI;

4. Platelet and Neutrophil Immunology Laboratory, BloodCenter of Wisconsin, Milwaukee, WI; and

5. Department of Medicine and

6. Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI

Abstract

Key Points Platelet-activating, but not nonactivating, human HIT antibodies bind to and activate PF4-treated platelets. Activating antibodies may recognize subtle conformational changes induced in PF4 by chondroitin-4-sulfate, the major platelet glycosaminoglycan.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/125/1/155/1383498/155.pdf

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4. Antibodies from patients with heparin-induced thrombocytopenia/thrombosis are specific for platelet factor 4 complexed with heparin or bound to endothelial cells.;Visentin;J Clin Invest,1994

5. Heparin-associated thrombocytopenia: isolation of the antibody and characterization of a multimolecular PF4-heparin complex as the major antigen.;Greinacher;Thromb Haemost,1994

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