ArticleNature communications2017
Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- HIT in the head: a systematic review of cerebral venous sinus thrombosis in classical and autoimmune heparin-induced thrombocytopenia.Journal of thrombosis and thrombolysis · 2021Pooled it
- Design of a modified platelet immunofluorescence test to assess platelet-reactive antibody burden and its association with platelet functional exhaustion and clinical features in chronic immune thrombocytopenia.British journal of haematology · 2026Article
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Adenoviral Inciting Antigen and Somatic Hypermutation in VITT.The New England journal of medicine · 2026Observational
- The hidden threat: understanding anti-PF4 disorders without proximate heparin exposure.Frontiers in immunology · 2026Review
- Reversible Platelet Aggregation Induced by Low-Temperature Storage in Heparinized Whole Blood Samples.Hematology reports · 2025Article
- Cooperative effect between anti-PF4/H and anti-PF4 antibodies increases cell activation and thrombotic risk in HIT.Blood advances · 2025Article
- Article
- Anti-Platelet factor 4 immunothrombosis-not just heparin and vaccine triggers.Research and practice in thrombosis and haemostasis · 2025Review
- Case Report: Anti-platelet factor 4 -mediated immunothrombosis in a patient with ANCA vasculitis - a shared mechanism of NETosis.Frontiers in immunology · 2025Article
- Reflecting on chiral chimeric cancer and microbes: ambidextrous metabolism-the real danger?Frontiers in cell and developmental biology · 2025Article
- Advances in our understanding of anti-PF4 related immunothrombosis.Frontiers in immunology · 2025Review
- Review
- The Binding of the SARS-CoV-2 Spike Protein to Platelet Factor 4: A Proposed Mechanism for the Generation of Pathogenic Antibodies.Biomolecules · 2024Article
- Article
- Autoimmune Heparin-Induced Thrombocytopenia.Journal of clinical medicine · 2023Review
- Cerebral venous thrombosis in patients with autoimmune disease, hematonosis or coronavirus disease 2019: Many familiar faces and some strangers.CNS neuroscience & therapeutics · 2023Review
- Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT)-Insights from Clinical Cases, In Vitro Studies and Murine Models.Journal of clinical medicine · 2023Review
- Laboratory Testing for Heparin-Induced Thrombocytopenia and Vaccine-Induced Immune Thrombotic Thrombocytopenia Antibodies: A Narrative Review.Seminars in thrombosis and hemostasis · 2023Review
- Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibodies recognizing complexes of the chemokine platelet factor 4 (PF4/CXCL4) and polyanions (P) opsonize PF4-coated bacteria hereby mediating bacterial host defense. A subset of these antibodies may activate platelets after binding to PF4/heparin complexes, causing the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT). In autoimmune-HIT, anti-PF4/P-antibodies activate platelets in the absence of heparin. Here we show that antibodies with binding forces of approximately 60-100 pN activate platelets in the presence of polyanions, while a subset of antibodies from autoimmune-HIT patients with binding forces ≥100 pN binds to PF4 alone in the absence of polyanions. These antibodies with high binding forces cluster PF4-molecules forming antigenic complexes which allow binding of polyanion-dependent anti-PF4/P-antibodies. The resulting immunocomplexes induce massive platelet activation in the absence of heparin. Antibody-mediated changes in endogenous proteins that trigger binding of otherwise non-pathogenic (or cofactor-dependent) antibodies may also be relevant in other antibody-mediated autoimmune disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.