ArticleNature communications2022
Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm.
Article in Nature communications, 2022. 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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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- Fufang Huangbo Formula mitigates myeloproliferative neoplasms by activating p53/p21 signaling axis and inhibiting STAT3 and NF-κB signaling pathways.Pharmaceutical science advances · 2026Article
- Non-invasive multiparametric characterization of essential thrombocythemia, premyelofibrosis, and overt myelofibrosis.Leukemia · 2026Article
- Inhibition of RhoA-mediated secretory autophagy in megakaryocytes mitigates myelofibrosis in mice.Nature communications · 2026Article
- Preserving thrombosis and life years in polycythemia vera: start by reading the biology of the disease.Haematologica · 2026Article
- Application of NanoString Technologies in Chronic Myeloid Leukemia, Essential Thrombocythemia, Primary Myelofibrosis, and Polycythemia Vera: A Pilot Study.Diagnostics (Basel, Switzerland) · 2026Article
- Review
- ZnO-Hydroxyapatite-Coated Ti-6Al-4V With Curcumin and Ginger Extract for Load-Bearing Implants.Journal of the American Ceramic Society. American Ceramic Society · 2026Article
- Non-invasive detection of bone marrow fibrosis in myeloproliferative neoplasms using cell-free RNA.iScience · 2026Article
- A proteogenomic gene signature defines prognostic subgroups highlighting PI3K/AKT/mTOR signaling pathway as a therapeutic vulnerability in myeloid malignancies.Cell communication and signaling : CCS · 2025Article
- `Inflammatory mediators differentially regulate megakaryopoiesis and thrombopoiesis in myelofibrosis and essential thrombocythemia.Scientific reports · 2025Article
- NLRP3-induced systemic inflammation controls the development of JAK2V617F mutant myeloproliferative neoplasms.Nature communications · 2025Article
- Preclinical efficacy of tasquinimod-based combinations in advanced myeloproliferative neoplasms in blastic phase.Blood advances · 2025Article
- Activation of integrin signaling up-regulates pro-inflammatory cytokines in JAK2-V617F positive hematopoietic cells.Cell communication and signaling : CCS · 2025Article
- Efficacy of a novel BCL-xL degrader, DT2216, in preclinical models of JAK2-mutated post-MPN AML.Blood · 2025Article
- Contributions of Noncardiac Organ-Heart Immune Crosstalk and Somatic Mosaicism to Heart Failure: Current Knowledge and Perspectives.Circulation research · 2025Review
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Article
- Folate metabolism in myelofibrosis: a missing key?Annals of hematology · 2025Review
- CXCR4-enriched T regulatory cells preferentially home to bone marrow and resolve inflammation.iScience · 2024Article
- Immune-dysregulation harnessing in myeloid neoplasms.Cancer medicine · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic inflammation is frequently associated with myeloproliferative neoplasms (MPN), but the role of inflammation in the pathogenesis of MPN remains unclear. Expression of the proinflammatory cytokine interleukin-1 (IL-1) is elevated in patients with MPN as well as in Jak2V617F knock-in mice. Here, we show that genetic deletion of IL-1 receptor 1 (IL-1R1) normalizes peripheral blood counts, reduces splenomegaly and ameliorates bone marrow fibrosis in homozygous Jak2V617F mouse model of myelofibrosis. Deletion of IL-1R1 also significantly reduces Jak2V617F mutant hematopoietic stem/progenitor cells. Exogenous administration of IL-1β enhances myeloid cell expansion and accelerates the development of bone marrow fibrosis in heterozygous Jak2V617F mice. Furthermore, treatment with anti-IL-1R1 antibodies significantly reduces leukocytosis and splenomegaly, and ameliorates bone marrow fibrosis in homozygous Jak2V617F mice. Collectively, these results suggest that IL-1 signaling plays a pathogenic role in MPN disease progression, and targeting of IL-1R1 could be a useful strategy for the treatment of myelofibrosis.
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