ArticleNature cell biology2016
Chronic interleukin-1 exposure drives haematopoietic stem cells towards precocious myeloid differentiation at the expense of self-renewal.
Article in Nature cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 482 papers, 2 of them syntheses that pooled it.
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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
482 citing papers in PubMed, 2 syntheses or guidelines pooled it, 688 citations in OpenAlex.
- Association between theCancer biology & therapy · 2024Pooled it
- Effects of fine particulate matter on bone marrow-conserved hematopoietic and mesenchymal stem cells: a systematic review.Experimental & molecular medicine · 2024Pooled it
- Acute interleukin-1β antagonism decreases systemic inflammation, increases GLP-1 release, and modulates insulin secretion in individuals with prediabetes.American journal of physiology. Endocrinology and metabolism · 2026Trial
- The IL-1β inhibitor canakinumab in previously treated lower-risk myelodysplastic syndromes: a phase 2 clinical trial.Nature communications · 2024Trial
- Severe hematopoietic stem cell inflammation compromises chronic granulomatous disease gene therapy.Cell reports. Medicine · 2023Trial
- The epigenetic-metabolic axis of trained immunity: dual roles in disease pathogenesis and intervention.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Activated protein C promotes hematopoietic stem and progenitor cell quiescence and engraftment.EMBO molecular medicine · 2026Article
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- The role of the microbiota in hematological malignancies: A narrative review of mechanisms and therapeutic potential.New microbes and new infections · 2026Review
- Activating an interleukin 4-FLT3-STAT6 axis in multipotent progenitors restores lymphopoiesis in inflammation and aging.Immunity · 2026Article
- Quantitative molecular cartography of emergency myelopoiesis reveals conserved modules of hematopoietic activation.Cell stem cell · 2026Article
- Atherosclerotic Cardiovascular Disease and Cancer.Immunological reviews · 2026Review
- A 2026 update on myelodysplastic neoplasms: current state, challenges and future directions.Nature reviews. Clinical oncology · 2026Review
- Skin-derived G-CSF activates pathological granulopoiesis upon psoriasis.EMBO molecular medicine · 2026Article
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- Myeloid-Derived Suppressor Cells in Inflammatory Arthritis.International journal of molecular sciences · 2026Review
- Epigenetic programming by H3K23ac defines lineage fate of Meg3Nature cell biology · 2026Article
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- HSPCs and TScience advances · 2026Article
422 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
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Haematopoietic stem cells (HSCs) maintain lifelong blood production and increase blood cell numbers in response to chronic and acute injury. However, the mechanism(s) by which inflammatory insults are communicated to HSCs and their consequences for HSC activity remain largely unknown. Here, we demonstrate that interleukin-1 (IL-1), which functions as a key pro-inflammatory 'emergency' signal, directly accelerates cell division and myeloid differentiation of HSCs through precocious activation of a PU.1-dependent gene program. Although this effect is essential for rapid myeloid recovery following acute injury to the bone marrow, chronic IL-1 exposure restricts HSC lineage output, severely erodes HSC self-renewal capacity, and primes IL-1-exposed HSCs to fail massive replicative challenges such as transplantation. Importantly, these damaging effects are transient and fully reversible on IL-1 withdrawal. Our results identify a critical regulatory circuit that tailors HSC responses to acute needs, and is likely to underlie deregulated blood homeostasis in chronic inflammation conditions.
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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.