ArticleHaematologica2019
Factor H interferes with the adhesion of sickle red cells to vascular endothelium: a novel disease-modulating molecule.
Article in Haematologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 45 citations in OpenAlex.
- Proteomic Analysis of Golden Sputum Reveals Pulmonary Complement Activation During Acute Chest Syndrome in Children With Sickle Cell Disease.American journal of hematology · 2026Article
- Comprehensive analysis of complement activation in a hydroxyurea-treated patient cohort with sickle cell disease.Blood advances · 2026Article
- Emerging pathways in thromboinflammation of sickle cell disease: novel findings in disease pathogenesis.Research and practice in thrombosis and haemostasis · 2025Review
- Complement is activated in patients with acute chest syndrome caused by sickle cell disease and represents a therapeutic target.Science translational medicine · 2025Article
- Can we use biomarkers to identify those at risk of acute pain from sickle cell disease?Expert review of hematology · 2024Review
- Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation.Blood · 2023Article
- Sickle cell disease is a risk factor for transplant-associated thrombotic microangiopathy in children.Blood advances · 2023Article
- Liver Disease and Sickle Cell Disease: Auto-Immune Hepatitis more than a Coincidence; A Systematic Review of the Literature.Mediterranean journal of hematology and infectious diseases · 2023Review
- MASP-2 and MASP-3 inhibitors block complement activation, inflammation, and microvascular stasis in a murine model of vaso-occlusion in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Evidence of protective effects of recombinant ADAMTS13 in a humanized model of sickle cell disease.Haematologica · 2022Article
- Acute haemolysis by cold antibody during SARS-CoV-2 infection in a patient with Evans syndrome: a case report and literature review.Blood transfusion = Trasfusione del sangue · 2022Review
- Article
- Multiple inducers of endothelial NOS (eNOS) dysfunction in sickle cell disease.American journal of hematology · 2021Review
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
- Tyrosine Phosphorylation Modulates Peroxiredoxin-2 Activity in Normal and Diseased Red Cells.Antioxidants (Basel, Switzerland) · 2021Article
- ADAMTS13 and von Willebrand factor assessment in steady state and acute vaso-occlusive crisis of sickle cell disease.Research and practice in thrombosis and haemostasis · 2021Article
- Complement Factor H Family Proteins Modulate Monocyte and Neutrophil Granulocyte Functions.Frontiers in immunology · 2021Article
- The Benefits of Complement Measurements for the Clinical Practice.Methods in molecular biology (Clifton, N.J.) · 2021Review
- Complement in Sickle Cell Disease: Are We Ready for Prime Time?Journal of blood medicine · 2021Review
- Current and novel therapies for the prevention of vaso-occlusive crisis in sickle cell disease.Therapeutic advances in hematology · 2020Review
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18 authors at 8 institutions in 4 countries.
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Abstract
Sickle cell disease is an autosomal recessive genetic red cell disorder with a worldwide distribution. Growing evidence suggests a possible involvement of complement activation in the severity of clinical complications of sickle cell disease. In this study we found activation of the alternative complement pathway with microvascular deposition of C5b-9 on skin biopsies from patients with sickle cell disease. There was also deposition of C3b on sickle red cell membranes, which is promoted locally by the exposure of phosphatidylserine. In addition, we showed for the first time a peculiar "stop-and-go" motion of sickle cell red blood cells on tumor factor-α-activated vascular endothelial surfaces. Using the C3b/iC3b binding plasma protein factor Has an inhibitor of C3b cell-cell interactions, we found that factor H and its domains 19-20 prevent the adhesion of sickle red cells to the endothelium, normalizing speed transition times of red cells. We documented that factor H acts by preventing the adhesion of sickle red cells to P-selectin and/or the Mac-1 receptor (CD11b/CD18), supporting the activation of the alternative pathway of complement as an additional mechanism in the pathogenesis of acute sickle cell related vaso-occlusive crises. Our data provide a rationale for further investigation of the potential contribution of factor H and other modulators of the alternative complement pathway with potential implications for the treatment of sickle cell disease.
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