ArticleBlood advances2021
Anti-inflammatory treatment in MPN: targeting TNFR1 and TNFR2 in JAK2-V617F-induced disease.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Fufang Huangbo Formula mitigates myeloproliferative neoplasms by activating p53/p21 signaling axis and inhibiting STAT3 and NF-κB signaling pathways.Pharmaceutical science advances · 2026Article
- Taste receptor downregulation in diet-induced obesity reveals circumvallate papillae-specific taste-inflammatory networks.Frontiers in nutrition · 2026Article
- Activation of integrin signaling up-regulates pro-inflammatory cytokines in JAK2-V617F positive hematopoietic cells.Cell communication and signaling : CCS · 2025Article
- Monocyte Involvement in the Pathogenesis of Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Review
- RIPK1: A Promising Target for Intervention Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- Neutrophil-specific expression of JAK2-V617F or CALRmut induces distinct inflammatory profiles in myeloproliferative neoplasia.Journal of hematology & oncology · 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
- Contributions of bone marrow monocytes/macrophages in myeloproliferative neoplasms with JAK2Annals of hematology · 2023Article
- Myeloproliferative neoplasms - blurring the lines between cancer and chronic inflammatory disorder.Frontiers in oncology · 2023Review
- Genetic Knock-out of TNFR1 and TNFR2 in a JAK2-V617F Polycythemia Vera Mouse Model.HemaSphere · 2022Article
- Thromboinflammation in Myeloproliferative Neoplasms (MPN)-A Puzzle Still to Be Solved.International journal of molecular sciences · 2022Review
- Anti-IL-6 cytokine treatment has no impact on elevated hematocrit or splenomegaly in a polycythemia vera mouse model.Blood advances · 2022Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic nonresolving inflammatory syndrome is a major disease feature in myeloproliferative neoplasms (MPNs). Systemic inflammation promotes the growth of the JAK2-V617F+ hematopoietic stem cell clone and is associated with constitutive symptoms (eg, fever, cachexia, and fatigue). Therefore, it is being discussed whether anti-inflammatory therapy, in addition to the well-established JAK inhibitor therapy, may be beneficial in the control of constitutive symptoms. Moreover, effective control of the inflammatory microenvironment may contribute to prevent transformation into secondary myelofibrosis and acute leukemia. Given the pivotal role of tumor necrosis factor α (TNF-α) in MPN and the distinct roles of TNF-α receptor 1 (TNFR1) and TNFR2 in inflammation, we investigated the therapeutic effects of αTNFR1 and αTNFR2 antibody treatment in MPN-like disease using the JAK2+/VF knock-in mouse model. Peripheral blood counts, bone marrow/spleen histopathology, and inflammatory cytokine levels in serum were investigated. αTNFR2 antibody treatment decreased white blood cells and modulated the serum levels of several cytokines [CXCL2, CXCL5, interleukin-12(p40)], as well as of macrophage colony-stimulating factor, but they lacked efficacy to ameliorate hematocrit and splenomegaly. αTNFR1 antibody treatment resulted in the mild suppression of elevated hematocrit of -10.7% and attenuated splenomegaly (22% reduction in spleen weight). In conclusion, our studies show that TNFR1 and TNFR2 play different roles in the biology of JAK2-V617F-induced disease that may be of relevance in future therapeutic settings.
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