ArticleBone marrow transplantation2010
CD49d blockade by natalizumab in patients with multiple sclerosis affects steady-state hematopoiesis and mobilizes progenitors with a distinct phenotype and function.
Article in Bone marrow transplantation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed, 56 citations in OpenAlex.
- Trial
- Enhanced pathogenicity of Th17 cells due to natalizumab treatment: Implications for MS disease rebound.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The results of a 24-month controlled, prospective study of relapsing multiple sclerosis patients at risk for progressive multifocal encephalopathy, who switched from prolonged use of natalizumab to teriflunomide.Multiple sclerosis journal - experimental, translational and clinical · 2021Article
- Adhesion Molecules Involved in Stem Cell Niche Retention During Normal Haematopoiesis and in Acute Myeloid Leukaemia.Frontiers in immunology · 2021Review
- Cytokine-induced hematopoietic stem and progenitor cell mobilization: unraveling interactions between stem cells and their niche.Annals of the New York Academy of Sciences · 2020Review
- Natalizumab in Multiple Sclerosis Treatment: From Biological Effects to Immune Monitoring.Frontiers in immunology · 2020Review
- Erythrocyte microRNAs show biomarker potential and implicate multiple sclerosis susceptibility genes.Clinical and translational medicine · 2020Article
- Host-Immune Interactions in JC Virus Reactivation and Development of Progressive Multifocal Leukoencephalopathy (PML).Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- Erythrocyte microRNA sequencing reveals differential expression in relapsing-remitting multiple sclerosis.BMC medical genomics · 2018Article
- Real-World Lab Data in Natalizumab Treated Multiple Sclerosis Patients Up to 6 Years Long-Term Follow Up.Frontiers in neurology · 2018Article
- New agents in HSC mobilization.International journal of hematology · 2017Review
- Host cell virus entry mechanisms enhance anti-JCV-antibody switch in natalizumab-treated multiple sclerosis patients.Journal of neurovirology · 2016Observational
- Enhanced Integrin α4β1-Mediated Adhesion Contributes to a Mobilization Defect of Endothelial Progenitor Cells in Diabetes.Diabetes · 2016Article
- Natalizumab Affects T-Cell Phenotype in Multiple Sclerosis: Implications for JCV Reactivation.PloS one · 2016Article
- Effects of Lycium barbarum Polysaccharides on Apoptosis, Cellular Adhesion, and Oxidative Damage in Bone Marrow Mononuclear Cells of Mice Exposed to Ionizing Radiation Injury.BioMed research international · 2016Article
- Hematopoietic mobilization: Potential biomarker of response to natalizumab in multiple sclerosis.Neurology · 2015Article
- Arsenic Primes Human Bone Marrow CD34+ Cells for Erythroid Differentiation.Bioinorganic chemistry and applications · 2015Article
- Long-term follow-up of peripheral lymphocyte subsets in a cohort of multiple sclerosis patients treated with natalizumab.Clinical and experimental immunology · 2014Article
- Infection-induced changes in hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
- Advances in stem cell mobilization.Blood reviews · 2014Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutic application of natalizumab, an anti-CD49d Ab, in patients with multiple sclerosis (MS) has been associated with increased levels of circulating CD34+ progenitors. We analyzed the frequency, phenotype and functional activity of CD34+ HSC in blood and BM of patients with MS who were treated with natalizumab. Compared with healthy controls and untreated MS patients, natalizumab treatment increased CD34+ cells in the peripheral blood 7-fold and in BM 10-fold. CD34+ cells derived from blood and marrow of natalizumab-treated patients expressed less of the stem cell marker CD133, were enriched for erythroid progenitors (CFU-E) and expressed lower levels of adhesion molecules than G-CSF-mobilized CD34+ cells. The level of surface CXCR-4 expression on CD34+ cells from patients treated with natalizumab was higher compared with that of CD34+ cells mobilized by G-CSF (median 43.9 vs 15.1%). This was associated with a more than doubled migration capacity toward a chemokine stimulus. Furthermore, CD34+ cells mobilized by natalizumab contained more mRNA for p21 and less for matrix metallopeptidase 9 compared with G-CSF-mobilized hematopoietic stem cell (HSC). Our data indicate that G-CSF and CD49d blockade mobilize different HSC subsets and suggest that both strategies may be differentially applied in specific cell therapy approaches.
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