ArticleCell reports2020
Interferon Gamma Mediates Hematopoietic Stem Cell Activation and Niche Relocalization through BST2.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
- IFN-γ induces hematopoietic stem cell myelopoiesis through Meis1 in tumor.Stem cell research & therapy · 2026Article
- Intra-Leukemic Interferon Signaling Suppresses Expansion and Mediates Chemoresistance in Human AML.Blood cancer discovery · 2026Article
- Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.Biomedicines · 2026Review
- Maternal acute SARS-CoV-2 infection impairs preimplantation embryo development and reprograms the early offspring hematopoietic system.Cell discovery · 2025Article
- Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity.Cancer cell · 2025Article
- CD317 stabilizes TNFR1 and confers the anti-inflammatory functions of MSCs via NF-κB/TSG6 pathway.Stem cell research & therapy · 2025Article
- Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells.Nature aging · 2025Article
- Computing hematopoiesis plasticity in response to genetic mutations and environmental stimulations.Life science alliance · 2025Article
- Single cell RNA sequencing improves the next generation of approaches to AML treatment: challenges and perspectives.Molecular medicine (Cambridge, Mass.) · 2025Review
- Conversion of placental hemogenic endothelial cells to hematopoietic stem and progenitor cells.Cell discovery · 2025Article
- Article
- Cellular stress and epigenetic regulation in adult stem cells.Life science alliance · 2024Review
- BST2 facilitates activation of hematopoietic stem cells through ERK signaling.Experimental hematology · 2024Article
- Bone Marrow and Peripheral Blood Mononuclear Cell Phenotype Changes after Cultivation and Autologous Infusion in Patients with Primary Biliary Cholangitis.Iranian journal of medical sciences · 2024Article
- Acute malaria suppresses the B lymphocytic niche in the bone marrow through the alteration of CXCL12-abundant reticular cells.International immunology · 2024Article
- Forged in the fire: Lasting impacts of inflammation on hematopoietic progenitors.Experimental hematology · 2024Review
- A Perfect Storm: The Convergence of Aging, Human Immunodeficiency Virus Infection, and Inflammasome Dysregulation.Current issues in molecular biology · 2024Review
- Article
- Oncostatin M: Dual Regulator of the Skeletal and Hematopoietic Systems.Current osteoporosis reports · 2024Review
- Bacterial-induced or passively administered interferon gamma conditions the lung for early control of SARS-CoV-2.Nature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
During chronic infection, the inflammatory cytokine interferon gamma (IFNγ) damages hematopoietic stem cells (HSCs) by disrupting quiescence and promoting excessive terminal differentiation. However, the mechanism by which IFNγ hinders HSC quiescence remains undefined. Using intravital 3-dimensional microscopy, we find that IFNγ disrupts the normally close interaction between HSCs and CXCL12-abundant reticular (CAR) cells in the HSC niche. IFNγ stimulation increases expression of the cell surface protein BST2, which we find is required for IFNγ-dependent HSC relocalization and activation. IFNγ stimulation of HSCs increases their E-selectin binding by BST2 and homing to the bone marrow, which depends on E-selectin binding. Upon chronic infection, HSCs from mice lacking BST2 are more quiescent and more resistant to depletion than HSCs from wild-type mice. Overall, this study defines a critical mechanism by which IFNγ promotes niche relocalization and activation in response to inflammatory stimulation and identifies BST2 as a key regulator of HSC quiescence. VIDEO ABSTRACT.
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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.