ArticleBlood2008
Immune complexes formed following the binding of anti-platelet factor 4 (CXCL4) antibodies to CXCL4 stimulate human neutrophil activation and cell adhesion.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin-induced thrombocytopenia.Blood advances · 2018Guideline
- Antibodies to platelet factor 4-heparin complex and outcome in hemodialysis patients with diabetes.Clinical journal of the American Society of Nephrology : CJASN · 2010Trial
- Insights Into the Role of Platelet Factor 4 in Neurodegenerative Diseases.CNS neuroscience & therapeutics · 2026Review
- Heparin: Over 100 Years of Anticoagulation.Handbook of experimental pharmacology · 2026Review
- Antiphospholipid syndrome (APS) is a platelet factor 4 (PF4)-centric immunothrombotic disorder.bioRxiv : the preprint server for biology · 2025Article
- Structural and functional changes underlying activation of monocytes in heparin-induced thrombocytopenia.Journal of thrombosis and haemostasis : JTH · 2025Article
- The Role of CXCL4 in Systemic Sclerosis: DAMP, Auto-Antigen and Biomarker.International journal of molecular sciences · 2025Review
- Complement activation as a biomarker for platelet-activating antibodies in heparin-induced thrombocytopenia.Journal of thrombosis and haemostasis : JTH · 2025Article
- Multi-omics analysis reveals neutrophil heterogeneity and key molecular drivers in sepsis-associated acute kidney injury.Frontiers in immunology · 2025Article
- Article
- A let-7 microRNA-RALB axis links the immune properties of iPSC-derived megakaryocytes with platelet producibility.Nature communications · 2024Article
- Review
- Treatment of thrombocytopenia and thrombosis in HIT in mice using deglycosylated KKO: a novel therapeutic?Blood advances · 2023Article
- Novel Knowledge about Molecular Mechanisms of Heparin-Induced Thrombocytopenia Type II and Treatment Targets.International journal of molecular sciences · 2023Review
- Treatment of drug-induced immune thrombocytopenias.Haematologica · 2022Review
- Insights Into Immunothrombotic Mechanisms in Acute Stroke due to Vaccine-Induced Immune Thrombotic Thrombocytopenia.Frontiers in immunology · 2022Article
- Complement mediates binding and procoagulant effects of ultralarge HIT immune complexes.Blood · 2021Article
- Vaccine induced thrombotic thrombocytopenia: The shady chapter of a success story.Metabolism open · 2021Article
- Cutaneous mucinosis of infancy: a rare case of joint involvement.Pediatric rheumatology online journal · 2021Article
- Heparin-Induced Thrombocytopenia: A Review of New Concepts in Pathogenesis, Diagnosis, and Management.Journal of clinical medicine · 2021Review
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 2 institutions in 1 country.
Funding
Abstract
We tested the possibility that immune complexes formed following platelet factor 4 (PF4/CXCL4) binding to anti-PF4 antibody can stimulate neutrophil activation, similar to previous reports with platelets. Monoclonal Abs against PF4 and IgG from a heparin-induced thrombocytopenia (HIT) patient were applied. We observed that although PF4 or anti-PF4 antibody alone did not alter neutrophil function, costimulation with both reagents resulted in approximately 3-fold increase in cell surface Mac-1 expression, enhanced cell adhesion via L-selectin and CD18 integrins, and degranulation of secondary and tertiary granules. The level of Mac-1 up-regulation peaked at an intermediate PF4 dose, suggesting that functional response varies with antigen-antibody stoichiometry. PF4 binding to neutrophils was blocked by chondroitinase ABC. Cell activation was inhibited by both chondroitinase ABC and anti-CD32/FcgammaRII blocking mAb, IV.3. Confocal microscopy demonstrated that immune complexes colocalize with CD32a. Studies with HIT IgG demonstrated that neutrophils could be activated in the absence of exogenous heparin. These data, together, show that leukocyte surface chondroitin sulfates promote neutrophil activation by enhancing immune-complex binding to CD32a. Studies with recombinant PF4 suggest a role for arginine 49 in stabilizing PF4-chondroitin binding. Neutrophils activated via this mechanism may contribute to thrombosis and inflammation in patients mounting an immune response to PF4-heparin.
Indexed as
Identifiers
What OpenQuestion holds
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.