ArticleNature communications2023
Clonal hematopoiesis related TET2 loss-of-function impedes IL1β-mediated epigenetic reprogramming in hematopoietic stem and progenitor cells.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 60 citations in OpenAlex.
- The IL-1β inhibitor canakinumab in previously treated lower-risk myelodysplastic syndromes: a phase 2 clinical trial.Nature communications · 2024Trial
- Second primary cancers following hematologic malignancies: Epidemiology, pathobiology and clinical management.Human vaccines & immunotherapeutics · 2026Review
- Auto-immune diseases associated with myelodysplastic syndrome and chronic myelomonocytic leukemia do not impact allogenic transplantation outcomes.Bone marrow transplantation · 2026Article
- Canakinumab or emavusertib for anemia in lower-risk MDS: results of the CANFIRE and LUCAS phase 2, open-label, multicenter trials.Communications medicine · 2026Article
- Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Stromal cell senescence augments haematopoietic cell fitness in clonal haematopoiesis.Nature cell biology · 2026Article
- Quantitative molecular cartography of emergency myelopoiesis reveals conserved modules of hematopoietic activation.Cell stem cell · 2026Article
- A 2026 update on myelodysplastic neoplasms: current state, challenges and future directions.Nature reviews. Clinical oncology · 2026Review
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026Review
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- Review
- TET2 loss enhances early response to inflammation in primitive and committed myeloid cells.Experimental hematology · 2026Article
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Clonal Hematopoiesis (CHIP) in Pulmonary Embolism and CTEPH: Evidence, Mechanisms, and Risk Stratification.International journal of molecular sciences · 2026Review
- Clonal hematopoiesis, inflammaging, and vascular disease: mechanisms, risk stratification, and therapeutic frontiers in older adults.Acta pharmacologica Sinica · 2026Article
- Cancer-Like Fragmentomic Characteristics of Somatic Variants in Cell-Free DNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epigenetic reactivation of the tumor suppressor ZBTB7A by KDM4 inhibition in human acute myeloid leukemia.Science translational medicine · 2026Article
- Hematopoietic stem cell aging promotesResearch square · 2026Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Clonal hematopoiesis (CH) is defined as a single hematopoietic stem/progenitor cell (HSPC) gaining selective advantage over a broader range of HSPCs. When linked to somatic mutations in myeloid malignancy-associated genes, such as TET2-mediated clonal hematopoiesis of indeterminate potential or CHIP, it represents increased risk for hematological malignancies and cardiovascular disease. IL1β is elevated in patients with CHIP, however, its effect is not well understood. Here we show that IL1β promotes expansion of pro-inflammatory monocytes/macrophages, coinciding with a failure in the demethylation of lymphoid and erythroid lineage associated enhancers and transcription factor binding sites, in a mouse model of CHIP with hematopoietic-cell-specific deletion of Tet2. DNA-methylation is significantly lost in wild type HSPCs upon IL1β administration, which is resisted by Tet2-deficient HSPCs, and thus IL1β enhances the self-renewing ability of Tet2-deficient HSPCs by upregulating genes associated with self-renewal and by resisting demethylation of transcription factor binding sites related to terminal differentiation. Using aged mouse models and human progenitors, we demonstrate that targeting IL1 signaling could represent an early intervention strategy in preleukemic disorders. In summary, our results show that Tet2 is an important mediator of an IL1β-promoted epigenetic program to maintain the fine balance between self-renewal and lineage differentiation during hematopoiesis.
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