ArticleInternational journal of molecular sciences2022
Phagocytosis of Erythrocytes from Gaucher Patients Induces Phenotypic Modifications in Macrophages, Driving Them toward Gaucher Cells.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Sphingolipids in Gaucher disease: a systematic review.Orphanet journal of rare diseases · 2025Pooled it
- Article
- Gaucher disease: the hematologist's perspective of a multisystemic disorder.Annals of hematology · 2026Review
- A Multiscale Signaling-Biophysical Framework Reveals Mechanisms of Macrophage-Mediated RBC Clearance in Sickle Cell and Gaucher Disease.bioRxiv : the preprint server for biology · 2026Article
- CD71Scandinavian journal of immunology · 2026Article
- In silico biophysics and rheology of blood and red blood cells in Gaucher Disease.PLoS computational biology · 2025Article
- Eryptosis in Liver Diseases: Contribution to Anemia and Hypercoagulation.Medical sciences (Basel, Switzerland) · 2025Review
- Reduced Erythrocyte Opsonization by Calreticulin, Lactadherin, Mannose-binding Lectin, and Thrombospondin-1 in MAFLD Patients.Cardiovascular & hematological disorders drug targets · 2025Article
- Molecular and Immunometabolic Landscape of Erythrophagocytosis-induced Ferroptosis.Cardiovascular & hematological disorders drug targets · 2025Review
- In silico biophysics and rheology of blood and red blood cells in Gaucher Disease.bioRxiv : the preprint server for biology · 2024Article
- A review on Gaucher disease: therapeutic potential of β-glucocerebrosidase-targeted mRNA/saRNA approach.International journal of biological sciences · 2024Review
- Physiology of Red Cell Lineage: From Erythroblast Progenitors to Mature Red Blood Cell.International journal of molecular sciences · 2023Article
- Article
- Hereditary Hyperferritinemia.International journal of molecular sciences · 2023Review
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Gaucher disease (GD) is caused by glucocerebrosidase deficiency leading to the accumulation of sphingolipids in macrophages named "Gaucher's Cells". These cells are characterized by deregulated expression of cell surface markers, abnormal secretion of inflammatory cytokines, and iron sequestration. These cells are known to infiltrate tissues resulting in hematological manifestations, splenomegaly, and bone diseases. We have already demonstrated that Gaucher red blood cells exhibit altered properties suggesting their key role in GD clinical manifestations. We hypothesized that Gaucher's erythrocytes could be prone to premature destruction by macrophages contributing to the formation of altered macrophages and Gaucher-like cells. We conducted in vitro experiments of erythrophagocytosis using erythrocytes from Gaucher's patients or healthy donors. Our results showed an enhanced erythrophagocytosis of Gaucher red blood cells compared to healthy red blood cells, which is related to erythrocyte sphingolipids overload and reduced deformability. Importantly, we showed elevated expression of the antigen-presenting molecules CD1d and MHC-II and of the iron-regulator hepcidin in macrophages, as well as enhanced secretion of the pro-inflammatory cytokine IL-1β after phagocytosis of GD erythrocytes. These results strongly suggested that erythrophagocytosis in GD contribute to phenotypic modifications in macrophages. This present study shows that erythrocytes-macrophages interactions may be crucial in GD pathophysiology and pathogenesis.
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