ArticleEuropean journal of immunology2015
CXCR4 antagonist AMD3100 redistributes leukocytes from primary immune organs to secondary immune organs, lung, and blood in mice.
Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 76 citations in OpenAlex.
- Ex vivo bone marrow subniches influence the fate of human antibody-secreting cells.Science advances · 2026Article
- Microglial state transitions dominate the brain immune response in the subacute phase after cardiac arrest.Journal of neuroinflammation · 2026Article
- AMD3100 modulates the secretome responses of human Mesenchymal Stromal Cells but not their inhibitory effect on T cell proliferation.Scientific reports · 2026Article
- The interrelationship between prostate cancer and osteoporosis: new perspectives on shared molecular pathways and treatment strategies.International journal of surgery (London, England) · 2026Article
- A CXCR4 partial agonist improves immunotherapy by targeting immunosuppressive neutrophils and cancer-driven granulopoiesis.Cancer cell · 2025Article
- Unveiling WHIM syndrome: Mavorixafor's emerging role in immune restoration and therapy.Clinical and experimental immunology · 2025Review
- Neutrophils in cancer: from biology to therapy.Cellular & molecular immunology · 2025Review
- CXCR4 antagonism corrects neutrophil abnormalities and reduces pneumonia severity in a pharmacological mouse model of CXCR2 loss-of-function-mediated neutropenia.Frontiers in immunology · 2025Article
- A Bioinformatics Investigation of Hub Genes Involved in Treg Migration and Its Synergistic Effects, Using Immune Checkpoint Inhibitors for Immunotherapies.International journal of molecular sciences · 2024Article
- Plerixafor for pathogen-agnostic treatment in murine thigh infection and zebrafish sepsis.Clinical and translational science · 2024Article
- Clostridioides difficile toxin B subverts germinal center and antibody recall responses by stimulating a drug-treatable CXCR4-dependent mechanism.Cell reports · 2024Article
- CXCR4 antagonism ameliorates leukocyte abnormalities in a preclinical model of WHIM syndrome.Frontiers in immunology · 2024Article
- Evolutionarily conserved mechanisms regulating stress-induced neutrophil redistribution in fish.Frontiers in immunology · 2024Article
- Intratumoral CXCR4Frontiers in immunology · 2024Article
- Severe CD8+ T Lymphopenia in WHIM Syndrome Caused by Selective Sequestration in Primary Immune Organs.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Soluble factors from TLR4- or TCR-activated cells contribute to stability of the resting phenotype and increase the expression of CXCR4 of human memory CD4 T cells.Immunologic research · 2023Article
- Neutrophil Heterogeneity and its Roles in the Inflammatory Network after Ischemic Stroke.Current neuropharmacology · 2023Article
- GZMKNature communications · 2022Article
- Loss of Parathyroid Hormone Receptor Signaling in Osteoprogenitors Is Associated With Accumulation of Multiple Hematopoietic Lineages in the Bone Marrow.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Chemokines as Regulators of Neutrophils: Focus on Tumors, Therapeutic Targeting, and Immunotherapy.Cancers · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
AMD3100 (plerixafor), is a specific CXCR4 antagonist approved by the FDA for mobilizing hematopoietic stem cells from bone marrow to blood for transplantation in cancer. AMD3100 also mobilizes most mature leukocyte subsets to blood; however, their source and trafficking potential have not been fully delineated. Here, we show that a single injection of AMD3100 10 mg/kg into C57Bl/6 mice rapidly mobilizes (peak ∼ 2.5 h) the same leukocyte subsets to blood as in humans. Using this model, we found that AMD3100 mobilization of neutrophils, lymphocytes, and monocytes to blood is not reduced by splenectomy or by blockade of lymphocyte egress from lymph node with FTY720, but is coupled to (i) reduced content of each of these cell types in the bone marrow; (ii) reduced T-cell numbers in thymuses; (iii) increased lymphocytes in lymph nodes; and (iv) increased neutrophil and monocyte content in the lung. Direct intrathymic labeling showed that AMD3100 selectively mobilizes naïve thymic CD4(+) and CD8(+) T cells to blood. Finally, AMD3100-induced neutrophil mobilization to blood did not reduce neutrophil trafficking to thioglycollate-inflamed peritoneum. Thus, AMD3100 redistributes lymphocytes, monocytes, and neutrophils from primary immune organs to secondary immune organs, peripheral tissues, and blood, without compromising neutrophil trafficking to inflamed sites.
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