ArticleSeminars in hematology2022
Pathogenesis of vaccine-induced immune thrombotic thrombocytopenia (VITT).
Article in Seminars in hematology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 63 citations in OpenAlex.
- Charge-driven antiviral responses enhance autoreactivity in severe COVID-19.Research square · 2026Article
- Immobilized IgG-containing immune complexes require platelets to recruit neutrophils during inflammation.The Journal of clinical investigation · 2026Article
- Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT)-like Syndrome: A Case Report and Some Considerations on a Novel Diagnostic and Therapeutic Challenge.Diagnostics (Basel, Switzerland) · 2026Article
- Review
- Vaxtherapy, a Multiphase Therapeutic Protocol Approach for Longvax, the COVID-19 Vaccine-Induced Disease: Spike Persistence as the Core Culprit and Its Downstream Effects.Diseases (Basel, Switzerland) · 2025Article
- Comparison of vaccine-induced immune thrombocytopenia and thrombosis cases following two adenovirus-vectored COVID-19 vaccines.Communications medicine · 2025Article
- Review
- Lipid signatures of immunothrombosis: insights from VITT.Research and practice in thrombosis and haemostasis · 2025Article
- Anti-Platelet factor 4 immunothrombosis-not just heparin and vaccine triggers.Research and practice in thrombosis and haemostasis · 2025Review
- The Crucial Roles of Platelets as Immune Mediators in Sepsis.Journal of inflammation research · 2025Review
- Thromboembolic Events in the Era of COVID-19: A Detailed Narrative Review.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025Review
- Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis - a shared mechanism of NETosis.Frontiers in immunology · 2025Article
- Thymidine phosphorylase mediates SARS-CoV-2 spike protein enhanced thrombosis in K18-hACE2Thrombosis research · 2024Article
- Evaluation of adenoviral vector Ad19a encoding RSV-F as novel vaccine against respiratory syncytial virus.NPJ vaccines · 2024Article
- Incidence and management of the main serious adverse events reported after COVID-19 vaccination.Pharmacology research & perspectives · 2024Review
- Outcomes After Decompressive Surgery for Severe Cerebral Venous Sinus Thrombosis Associated or Not Associated with Vaccine-Induced Immune Thrombosis with Thrombocytopenia: A Multicenter Cohort Study.Neurocritical care · 2024Article
- Vaccine-Induced Immune Thrombotic Thrombocytopenia: Clinicopathologic Features and New Perspectives on Anti-PF4 Antibody-Mediated Disorders.Journal of clinical medicine · 2024Review
- Article
- Review
- Comparison of Venous Thromboembolism Outcomes after COVID-19 and Influenza Vaccinations.TH open : companion journal to thrombosis and haemostasis · 2023Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vaccine-induced immune thrombotic thrombocytopenia (VITT; synonym, thrombosis with thrombocytopenia syndrome, is associated with high-titer immunoglobulin G antibodies directed against platelet factor 4 (PF4). These antibodies activate platelets via platelet FcγIIa receptors, with platelet activation greatly enhanced by PF4. Here we summarize the current concepts in the pathogenesis of VITT. We first address parallels between heparin-induced thrombocytopenia and VITT, and provide recent findings on binding of PF4 to adenovirus particles and non-assembled adenovirus proteins in the 2 adenovirus vector-based COVID-19 vaccines, ChAdOx1 nCoV-19 and Ad26.COV2.S. Further, we discuss the potential role of vaccine constituents such as glycosaminoglycans, EDTA, polysorbate 80, human cell-line proteins and nucleotides as potential binding partners of PF4. The immune response towards PF4 in VITT is likely triggered by a proinflammatory milieu. Human cell-line proteins, non-assembled virus proteins, and potentially EDTA may contribute to the proinflammatory state. The transient nature of the immune response towards PF4 in VITT makes it likely that-as in heparin-induced thrombocytopenia -marginal zone B cells are key for antibody production. Once high-titer anti-PF4 antibodies have been formed 5 to 20 days after vaccination, they activate platelets and granulocytes. Activated granulocytes undergo NETosis and the released DNA also forms complexes with PF4, which fuels the Fcγ receptor-dependent cell activation process, ultimately leading to massive thrombin generation. Finally, we summarize our initial observations indicating that VITT-like antibodies might also be present in rare patients with recurrent venous and arterial thrombotic complications, independent of vaccination.
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