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. 2022 Oct 15;29:82. doi: 10.1186/s12929-022-00853-8

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Potential mechanism of VITT. After vaccination, the viral proteins in the vaccine components might bind with PF4, thereby forming epitopes that can be recognized by the immune system and inducing the generation of anti-PF4 antibodies. Anti-PF4 antibodies form immune complexes with PF4 and bind with the Fc receptor on the surface of the platelet, leading to platelet activation and aggregation, and finally VITT 5 to 20 days after vaccination. (Created with BioRender.com)