ArticleBlood advances2019
Defective negative regulation of Toll-like receptor signaling leads to excessive TNF-α in myeloproliferative neoplasm.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 71 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
- Inflammatory and Immune Microenvironment in Myeloproliferative Neoplasms: Pathogenic Mechanisms and Therapeutic Opportunities.Cancers · 2026Review
- Positive and Negative Cardiovascular Effects of JAK Inhibitors in Inflammation.ACR open rheumatology · 2026Review
- Integrated transcriptome-proteome analysis in patients with myelofibrosis-related anemia.Annals of hematology · 2026Article
- The Intricate Dance Between Inflammation and Myeloproliferative Neoplasms: From Origins to Outcomes.Current hematologic malignancy reports · 2026Review
- The JAK2V617F and CALR mutations and risk of cancer, cardiovascular diseases, and all-cause mortality.Journal of internal medicine · 2026Article
- Machine learning identifies inflammation-related diagnostic biomarkers for primary myelofibrosis with clinical validation.Scientific reports · 2025Article
- TNF-α impairs platelet function by inhibiting autophagy and disrupting metabolism via syntaxin 17 downregulation.The Journal of clinical investigation · 2025Article
- Monocyte Involvement in the Pathogenesis of Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Review
- Article
- Transcriptomic profiling identifies ferroptosis and NF-κB signaling involved in α-dimorphecolic acid regulation of microglial inflammation.Journal of translational medicine · 2025Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- JAK Inhibitors for Myelofibrosis: Strengths and Limitations.Current hematologic malignancy reports · 2024Review
- Immune-dysregulation harnessing in myeloid neoplasms.Cancer medicine · 2024Review
- Inherited polygenic effects on common hematological traits influence clonal selection on JAK2Nature genetics · 2024Article
- Elevated levels of damage-associated molecular patterns HMGB1 and S100A8/A9 coupled with toll-like receptor-triggered monocyte activation are associated with inflammation in patients with myelofibrosis.Frontiers in immunology · 2024Article
- TNF-α is a predictive marker in distinguishing myeloproliferative neoplasm and idiopathic erythrocytosis/thrombocytosis: development and validation of a non-invasive diagnostic model.Frontiers in oncology · 2024Article
- The impact of gut microbial signals on hematopoietic stem cells and the bone marrow microenvironment.Frontiers in immunology · 2024Review
- Molecular Studies for the Early Detection of Philadelphia-Negative Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Contributions of bone marrow monocytes/macrophages in myeloproliferative neoplasms with JAK2Annals of hematology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Patients with myeloproliferative neoplasms (MPN) have high levels of inflammatory cytokines, some of which drive many of the debilitating constitutional symptoms associated with the disease and may also promote expansion of the neoplastic clone. We report here that monocytes from patients with MPN have defective negative regulation of Toll-like receptor (TLR) signaling that leads to unrestrained production of the inflammatory cytokine tumor necrosis factor α (TNF-α) after TLR activation. Specifically, monocytes of patients with MPN are insensitive to the anti-inflammatory cytokine interleukin 10 (IL-10) that negatively regulates TLR-induced TNF-α production. This inability to respond to IL-10 is a not a direct consequence of
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