ArticleOncoimmunology2020
The role of circulating monocytes and JAK inhibition in the infectious-driven inflammatory response of myelofibrosis.
Article in Oncoimmunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Multi-parametric profiling of plasma-derived extracellular vesicles reveals a disease-associated molecular signature supporting a liquid biopsy approach in myelofibrosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Monocyte Involvement in the Pathogenesis of Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Review
- Platelet activation stimulates macrophages to enhance ulcerative colitis through PF4/CXCR3 signaling.International journal of molecular medicine · 2025Article
- Article
- Pluronic F127/lecithin PLGA nanoparticles as carriers of monocyte-targeted jakinibs: a potential therapeutic platform.Nanomedicine (London, England) · 2025Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- JAK/STAT signaling pathway affects CCR5 expression in human CD4Science advances · 2024Article
- Functionally Relevant Cytokine/Receptor Axes in Myelofibrosis.Biomedicines · 2023Review
- Contributions of bone marrow monocytes/macrophages in myeloproliferative neoplasms with JAK2Annals of hematology · 2023Article
- Extracellular vesicles in hematological malignancies: EV-dence for reshaping the tumoral microenvironment.Frontiers in immunology · 2023Review
- Brucellosis complicated by myelofibrosis: report of five cases and review of literature.International journal of clinical and experimental pathology · 2023Article
- Insights gained from single-cell analysis of immune cells in tofacitinib treatment of Vogt-Koyanagi-Harada disease.JCI insight · 2022Article
- Philadelphia-negative myeloproliferative neoplasms display alterations in monocyte subpopulations frequency and immunophenotype.Medical oncology (Northwood, London, England) · 2022Article
- Transcriptional differences between JAK2-V617F and wild-type bone marrow cells in patients with myeloproliferative neoplasms.Experimental hematology · 2022Article
- Cryptococcal infection with ruxolitinib in primary myelofibrosis: A case report and literature review.Clinical case reports · 2022Article
- Bone Marrow Niches and Tumour Cells: Lights and Shadows of a Mutual Relationship.Frontiers in immunology · 2022Review
- Trial Watch: combination of tyrosine kinase inhibitors (TKIs) and immunotherapy.Oncoimmunology · 2022Review
- Philadelphia-Negative Chronic Myeloproliferative Neoplasms during the COVID-19 Pandemic: Challenges and Future Scenarios.Cancers · 2021Review
- Review
- COVID-19 as a mediator of interferon deficiency and hyperinflammation: Rationale for the use of JAK1/2 inhibitors in combination with interferon.Cytokine & growth factor reviews · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelofibrosis (MF) is characterized by chronic inflammation and hyper-activation of the JAK-STAT pathway. Infections are one of the main causes of morbidity/mortality. Therapy with Ruxolitinib (RUX), a JAK1/2 inhibitor, may further increase the infectious risk. Monocytes are critical players in inflammation/immunity through cytokine production and release of bioactive extracellular vesicles. However, the functional behavior of MF monocytes, particularly during RUX therapy, is still unclear. In this study, we found that monocytes from JAK2V617F-mutated MF patients show an altered expression of chemokine (CCR2, CXCR3, CCR5) and cytokine (TNF-α-R, IL10-R, IL1β-R, IL6-R) receptors. Furthermore, their ability to produce and secrete free and extracellular vesicles-linked cytokines (IL1β, TNF-α, IL6, IL10) under lipopolysaccharides (LPS) stimulation is severely impaired. Interestingly, monocytes from RUX-treated patients show normal level of chemokine, IL10, IL1β, and IL6 receptors together with a restored ability to produce intracellular and to secrete extracellular vesicles-linked cytokines after LPS stimulation. Conversely, RUX therapy does not normalize TNF-R1/2 receptors expression and the LPS-driven secretion of free pro/anti-inflammatory cytokines. Accordingly, upon LPS stimulation,
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