FcγRIIa - dependent platelet activation identified in COVID-19 vaccine-induced immune thrombotic thrombocytopenia-, heparin-induced thrombocytopenia, streptokinase- and anisoylated plasminogen-streptokinase activator complex-induced platelet activation
- 1Department of Medical Sciences and Education, Boston University School of Medicine, Boston, MA, United States
- 2School of Medicine, The Royal College of Surgeons in Ireland, Medical University of Bahrain, Al Sayh, Muharraq Governorate, Bahrain
A Corrigendum on
by Abdelouahed, M., Yateem, D., and Fredericks, S. (2023). Front. Cardiovasc. Med. 10:1282637. doi: 10.3389/fcvm.2023.1282637
In the published article, there was an error in Figure 1 as published. The incorrect image for Figure 1 was used. The corrected figure appears below.
Figure 1. Vaccine-induced immune thrombotic thrombocytopenia (VITT). Antibodies induce platelet aggregation through FcγRIIa. SARS-CoV-2 virions, or its spike protein, produced after COVID-19 vaccination, bind to platelets via ACE2 receptor, leading to activation of platelets and the secretion of platelet factor 4 (PF4). PF4 then biochemically associates with the spike protein, forming PF4-Spike complexes that stimulate VITT anti-PF4 antibody production. VITT pathological IgG antibodies induce platelet aggregation through platelet FcγRIIa and thrombocytopenia through platelet destruction by splenic macrophages.
In the published article, there was an error in Figure 3 as published. The incorrect image for Figure 3 was used. The corrected figure appears below.
Figure 3. Streptokinase (SK) and Anisoylated Plasminogen-Streptokinase Activator Complex (APSAC) induced platelet aggregation through FcγRIIa. Both Streptokinase and APSAC modify in vitro platelet aggregation by two mechanisms; reduced aggregation due to fibrinogenolysis, and enhanced aggregation via an immunological reaction. The reduced aggregation by SK (or APSAC) is mediated by plasmin generation and the fibrinogen degradation product, fragment E. As shown in this figure, SK (or APSAC) may also trigger platelet aggregation by a mechanism involving specific IgG anti-SK. Both SK- (or APSAC) induced platelet aggregation and SK- (or APSAC) enhanced ADP-induced platelet aggregation require the interaction of the Fc domain of the anti-SK antibodies with the platelet FcγRIIA.
The authors apologize for these errors and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Keywords: platelet activation, COVID-19, vaccine induced immune thrombotic thrombocytopenia, vaccination, FcγRIIa
Citation: Abdelouahed M, Yateem D and Fredericks S (2023) Corrigendum: FcγRIIa—dependent platelet activation identified in COVID-19 vaccine-induced immune thrombotic thrombocytopenia-, heparininduced thrombocytopenia, streptokinase- and anisoylated plasminogen-streptokinase activator complex-induced platelet activation. Front. Cardiovasc. Med. 10:1342177. doi: 10.3389/fcvm.2023.1342177
Received: 21 November 2023; Accepted: 27 November 2023;
Published: 6 December 2023.
Approved by: Frontiers Editorial Office, Frontiers Media SA, Switzerland
© 2023 Abdelouahed, Yateem and Fredericks. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Salim Fredericks c2ZyZWRlcmlja3NAcmNzaS1tdWIuY29t