ReviewFrontiers in immunology2016
Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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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
37 citing papers in PubMed, 62 citations in OpenAlex.
- Ruxolitinib reduces macrophage pyroptosis in aplastic anaemia.Clinical and experimental medicine · 2026Article
- Rare epigenetic alterations are conserved across hematopoietic differentiation stages after mycobacterial infection.JCI insight · 2026Article
- The gut microbiota limits systemic inflammation during neurotrophic viral CNS infection by priming tonic type I interferon signaling.Journal of neuroinflammation · 2025Article
- Latent Human Cytomegalovirus Infection Activates the STING Pathway but p-IRF3 Translocation Is Limited.Viruses · 2025Article
- Article
- Long-Term Follow-Up of Eltrombopag Treatment for Patients with Cyclosporin A Refractory/Relapsed Transfusion-Dependent Non-Severe Aplastic Anemia: A Report from a Single Center in China.Acta haematologica · 2025Article
- Platelets as a potential new immune coordinator in T cell-mediated aplastic anemia.Frontiers in oncology · 2025Review
- Unbiased Single-Cell Sequencing of Hematopoietic and Immune Cells from Aplastic Anemia Reveals the Contributors of Hematopoiesis Failure and Dysfunctional Immune Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Retrospective identification of the first cord blood-transplanted severe aplastic anemia in aFrontiers in immunology · 2024Review
- Single-cell transcriptomic analysis of hematopoietic progenitor cells from patients with systemic lupus erythematosus reveals interferon-inducible reprogramming in early progenitors.Frontiers in immunology · 2024Article
- Clinical Signs and Treatment of New-Onset Bone Marrow Failure Associated SARS-CoV-2 Infection in Children: A Single Institution Prospective Cohort Study.Mediterranean journal of hematology and infectious diseases · 2024Article
- Review
- 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
- SOCS1 Haploinsufficiency Presenting as Severe Enthesitis, Bone Marrow Hypocellularity, and Refractory Thrombocytopenia in a Pediatric Patient with Subsequent Response to JAK Inhibition.Journal of clinical immunology · 2022Article
- Age and Sex Divergence in Hematopoietic Radiosensitivity in Aged Mouse Models of the Hematopoietic Acute Radiation Syndrome.Radiation research · 2022Article
- Pre-exposure to mRNA-LNP inhibits adaptive immune responses and alters innate immune fitness in an inheritable fashion.PLoS pathogens · 2022Article
- Pre-exposure to mRNA-LNP inhibits adaptive immune responses and alters innate immune fitness in an inheritable fashion.bioRxiv : the preprint server for biology · 2022Article
- Clinical features, pathophysiology, and therapy of poor graft function post-allogeneic stem cell transplantation.Blood advances · 2022Review
- TIRAP drives myelosuppression through an Ifnγ-Hmgb1 axis that disrupts the endothelial niche in mice.The Journal of experimental medicine · 2022Article
- JAK inhibition in a patient with a STAT1 gain-of-function variant reveals STAT1 dysregulation as a common feature of aplastic anemia.Med (New York, N.Y.) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aplastic anemia (AA) occurs when the bone marrow fails to support production of all three lineages of blood cells, which are necessary for tissue oxygenation, infection control, and hemostasis. The etiology of acquired AA is elusive in the vast majority of cases but involves exhaustion of hematopoietic stem cells (HSC), which are usually present in the bone marrow in a dormant state, and are responsible for lifelong production of all cells within the hematopoietic system. This destruction is immune mediated and the role of interferons remains incompletely characterized. Interferon gamma (IFNγ) has been associated with AA and type I IFNs (alpha and beta) are well documented to cause bone marrow aplasia during viral infection. In models of infection and inflammation, IFNγ activates HSCs to differentiate and impairs their ability to self-renew, ultimately leading to HSC exhaustion. Recent evidence demonstrating that IFNγ also impacts the HSC microenvironment or niche, raises new questions regarding how IFNγ impairs HSC function in AA. Immune activation can also elicit type I interferons, which may exert effects both distinct from and overlapping with IFNγ on HSCs. IFNα/β increase HSC proliferation in models of sterile inflammation induced by polyinosinic:polycytidylic acid and lead to BM aplasia during viral infection. Moreover, patients being treated with IFNα exhibit cytopenias, in part due to BM suppression. Herein, we review the current understanding of how interferons contribute to the pathogenesis of acquired AA, and we explore additional potential mechanisms by which interferons directly and indirectly impair HSCs. A comprehensive understanding of how interferons impact hematopoiesis is necessary in order to identify novel therapeutic approaches for treating AA patients.
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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.