ArticleThe Journal of experimental medicine2014
Re-entry into quiescence protects hematopoietic stem cells from the killing effect of chronic exposure to type I interferons.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 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.
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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
204 citing papers in PubMed, 317 citations in OpenAlex.
- HIV is associated with an increased risk of age-related clonal hematopoiesis among older adults.Nature medicine · 2021Trial
- Type 1 interferon perturbates clonal competition by reshaping human blood development.Nature genetics · 2026Article
- Bone marrow myelopoiesis dysfunction in Alzheimer's disease limits monocyte homing to the brain and drives disease progression.Nature neuroscience · 2026Article
- Hematopoietic Stem Cell Metabolism during Stress and Aging.Advances in geriatric medicine and research · 2026Article
- Quantitative molecular cartography of emergency myelopoiesis reveals conserved modules of hematopoietic activation.Cell stem cell · 2026Article
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- Inflammation perturbs hematopoiesis by remodeling specific compartments of the bone marrow niche.Blood · 2026Article
- Lack of MDA5 delays hematopoietic aging by modulating inflammaging and proteostasis in mice.Nature communications · 2026Article
- Ruxolitinib reduces macrophage pyroptosis in aplastic anaemia.Clinical and experimental medicine · 2026Article
- An inflammatory and quiescent HSC subpopulation expands with age in humans.Genome biology · 2026Article
- IL-27 limits HSPC differentiation during infection and protects from stem cell exhaustion.eLife · 2025Article
- Article
- Space-associated stem cell hallmarks of aging and resilience in astronauts.Cell stem cell · 2025Article
- TLR2 agonism suppresses myeloid leukemogenesis by reprogramming leukemia stem cells.Blood advances · 2025Article
- Bcl-xL inhibition potentiates interferon-induced apoptosis in MPN stem cells.Blood advances · 2025Article
- The Dual Role of Interferon Signaling in Myeloproliferative Neoplasms: Pathogenesis and Targeted Therapeutics.Cancers · 2025Review
- IFN-I-Mediated Transcriptional Reprogramming Drives Myeloid-skewed Hematopoiesis in Sickle Cell Anemia.Research square · 2025Article
- Article
- An Inflammatory and Quiescent HSC Subpopulation Expands with Age in Humans.bioRxiv : the preprint server for biology · 2025Article
144 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Type I interferons (IFN-1s) are antiviral cytokines that suppress blood production while paradoxically inducing hematopoietic stem cell (HSC) proliferation. Here, we clarify the relationship between the proliferative and suppressive effects of IFN-1s on HSC function during acute and chronic IFN-1 exposure. We show that IFN-1-driven HSC proliferation is a transient event resulting from a brief relaxation of quiescence-enforcing mechanisms in response to acute IFN-1 exposure, which occurs exclusively in vivo. We find that this proliferative burst fails to exhaust the HSC pool, which rapidly returns to quiescence in response to chronic IFN-1 exposure. Moreover, we demonstrate that IFN-1-exposed HSCs with reestablished quiescence are largely protected from the killing effects of IFNs unless forced back into the cell cycle due to culture, transplantation, or myeloablative treatment, at which point they activate a p53-dependent proapoptotic gene program. Collectively, our results demonstrate that quiescence acts as a safeguard mechanism to ensure survival of the HSC pool during chronic IFN-1 exposure. We show that IFN-1s can poise HSCs for apoptosis but induce direct cell killing only upon active proliferation, thereby establishing a mechanism for the suppressive effects of IFN-1s on HSC function.
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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.