ArticleExperimental hematology2023
Inhibition of CXCR1/2 reduces the emperipolesis between neutrophils and megakaryocytes in the Gata1
Article in Experimental hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
The trial behind it
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Megakaryocytes Internalize and Are Activated by Immune Complexes.Circulation research · 2026Article
- Neutrophils as critical orchestrators of chronic inflammation.Cellular & molecular immunology · 2026Review
- Genetic deletion of P-selectin prevents fibrosis development by inhibiting the neutrophil megakaryocyte emperipolesis in the Gata1European journal of histochemistry : EJH · 2025Article
- Article
- New insights into the generation and function of megakaryocytes in health and disease.Haematologica · 2025Review
- Review
- Targeting innate and adaptive immunity to suppress lung cancer metastasis.Frontiers in immunology · 2025Review
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- CXCL8 and its cognate receptors CXCR1/CXCR2 in primary myelofibrosis.Haematologica · 2024Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Emperipolesis between neutrophils and megakaryocytes was first identified by transmission electron microscopy. Although rare under steady-state conditions, its frequency greatly increases in myelofibrosis, the most severe of myeloproliferative neoplasms, in which it is believed to contribute to increasing the transforming growth factor (TGF)-β microenvironmental bioavailability responsible for fibrosis. To date, the challenge of performing studies by transmission electron microscopy has hampered the study of factors that drive the pathological emperipolesis observed in myelofibrosis. We established a user-friendly confocal microscopy method that detects emperipolesis by staining with CD42b, specifically expressed on megakaryocytes, coupled with antibodies that recognize the neutrophils (Ly6b or neutrophil elastase antibody). With such an approach, we first confirmed that the bone marrow from patients with myelofibrosis and from Gata1
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Registered trials
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