ArticleHaematologica2018
Hematopoietic stem cell loss and hematopoietic failure in severe aplastic anemia is driven by macrophages and aberrant podoplanin expression.
Article in Haematologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Bone Marrow Failure Model Mimics Aplastic Anemia Patients: Single-Cell Landscape of Immune Response Reveals Novel Mechanisms of Immune Imbalance in AA.Cancer medicine · 2026Article
- Macrophages in Hematopoiesis and Related Blood Diseases.Genomics, proteomics & bioinformatics · 2025Review
- Macrophage polarization, inflammatory monocytes, and impaired MDSCs are associated with murine and human immune aplastic anemia.Journal of leukocyte biology · 2025Article
- Dynamic hierarchical ligand anisotropy for competing macrophage regulationBioactive materials · 2025Article
- Platelets as a potential new immune coordinator in T cell-mediated aplastic anemia.Frontiers in oncology · 2025Review
- Resolvin E1 improves efferocytosis and rescues severe aplastic anemia in mice.Cell death & disease · 2024Article
- The role of TIM3Journal of translational internal medicine · 2024Article
- Repair of dysfunctional bone marrow endothelial cells alleviates aplastic anemia.Science China. Life sciences · 2023Article
- Immunosuppressive Activity of Exosomes from Granulocytic Myeloid-Derived Suppressor Cells in a Murine Model of Immune Bone Marrow Failure.International journal of molecular sciences · 2023Article
- Resolvin E1 improves efferocytosis and rescues severe aplastic anemia in mice.bioRxiv : the preprint server for biology · 2023Article
- A novel inducible haematopoietic cell-depleting mouse model for chimeric complementation of blood cells.Cell proliferation · 2023Article
- Bone marrow expression of CD68/CD163 macrophages, IL-17 and FOXP3 cells in aplastic anemia and their relation to prognosis.European journal of haematology · 2023Article
- Spatial proteomics identifies a spectrum of immune dysregulation in acquired bone marrow failure syndromes.Frontiers in immunology · 2023Article
- Diversity in the bone marrow niche: Classic and novel strategies to uncover niche composition.British journal of haematology · 2022Review
- Liposomes trigger bone marrow niche macrophage "foam" cell formation and affect hematopoiesis in mice.Journal of lipid research · 2022Article
- Article
- Deleterious effect of bone marrow-resident macrophages on hematopoietic stem cells in response to total body irradiation.Blood advances · 2022Article
- The role of inflammation in hematopoiesis and bone marrow failure: What can we learn from mouse models?Frontiers in immunology · 2022Review
- CCR5 maintains macrophages in the bone marrow and drives hematopoietic failure in a mouse model of severe aplastic anemia.Leukemia · 2021Article
- Ultrastructural alterations of megakaryocytes in thrombocytopenia: A review of 43 cases.Blood science (Baltimore, Md.) · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Severe aplastic anemia (SAA) results from profound hematopoietic stem cell loss. T cells and interferon gamma (IFNγ) have long been associated with SAA, yet the underlying mechanisms driving hematopoietic stem cell loss remain unknown. Using a mouse model of SAA, we demonstrate that IFNγ-dependent hematopoietic stem cell loss required macrophages. IFNγ was necessary for bone marrow macrophage persistence, despite loss of other myeloid cells and hematopoietic stem cells. Depleting macrophages or abrogating IFNγ signaling specifically in macrophages did not impair T-cell activation or IFNγ production in the bone marrow but rescued hematopoietic stem cells and reduced mortality. Thus, macrophages are not required for induction of IFNγ in SAA and rather act as sensors of IFNγ. Macrophage depletion rescued thrombocytopenia, increased bone marrow megakaryocytes, preserved platelet-primed stem cells, and increased the platelet-repopulating capacity of transplanted hematopoietic stem cells. In addition to the hematopoietic effects, SAA induced loss of non-hematopoietic stromal populations, including podoplanin-positive stromal cells. However, a subset of podoplanin-positive macrophages was increased during disease, and blockade of podoplanin in mice was sufficient to rescue disease. Our data further our understanding of disease pathogenesis, demonstrating a novel role for macrophages as sensors of IFNγ, thus illustrating an important role for the microenvironment in the pathogenesis of SAA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.