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Haematologica. 2019 Jun;104(6):1237-1243. doi: 10.3324/haematol.2018.211086. Epub 2019 Mar 28.

Glycoprotein V is a relevant immune target in patients with immune thrombocytopenia.

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Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany.
Center for Clinical Transfusion Medicine, Medical Faculty of Tübingen, Eberhard Karls University, Tübingen, Germany.
The Canadian Blood Services & The Keenan Research Centre of St. Michael's Hospital, Toronto, ON, Canada.
Faculty for Chemistry and Biology, Fresenius University of Applied Sciences, Idstein, Germany.
IVth Department of Internal Medicine (Hematology/Oncology), Justus Liebig University, Giessen, Germany.
Department of Pathology and Laboratory Medicine, University of Rochester, NY, USA.
Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany
Center for Transfusion Medicine and Hemotherapy and Hemostasis Center, University Hospital Giessen and Marburg, Marburg, Germany.


Platelet autoantibody-induced platelet clearance represents a major pathomechanism in immune thrombocytopenia (ITP). There is growing evidence for clinical differences between anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib/IX mediated ITP. Glycoprotein V is a well characterized target antigen in Varicella-associated and drug-induced thrombocytopenia. We conducted a systematic study assessing the prevalence and functional capacity of autoantibodies against glycoprotein V. A total of 1140 patients were included. In one-third of patients, platelet-bound autoantibodies against glycoproteins Ib/IX, IIb/IIIa, or V were detected in a monoclonal antibody immobilization of platelet antigen assay; platelet-bound autoantiglycoprotein V was present in the majority of samples (222 out of 343, 64.7%). Investigation of patient sera revealed the presence of free autoantibodies against glycoprotein V in 13.5% of these patients by an indirect monoclonal antibody immobilization of platelet antigen assay, but in 39.6% by surface plasmon resonance technology. These antibodies showed significantly lower avidity (association/dissociation ratio 0.32±0.13 vs 0.73±0.14; P<0.001). High- and low-avidity antibodies induced comparable amounts of platelet uptake in a phagocytosis assay using CD14+ positively-selected human macrophages [mean phagocytic index, 6.81 (range, 4.75-9.86) vs 6.01 (range, 5.00-6.98); P=0.954]. In a NOD/SCID mouse model, IgG prepared from both types of anti-glycoprotein V autoantibodies eliminated human platelets with no detectable difference between the groups from the murine circulation [mean platelet survival at 300 minutes, 40% (range, 27-55) vs 35% (16-46); P=0.025]. Our data establish glycoprotein V as a relevant immune target in immune thrombocytopenia. We would suggest that further studies including glycoprotein V will be required before ITP treatment can be tailored according to platelet autoantibody specificity.

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