ArticleThe Journal of clinical investigation2015
IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 90 citations in OpenAlex.
- IRAK signaling in cancers: mechanisms, targeting, and clinical implications.Expert opinion on investigational drugs · 2025Review
- ST2/IL-33 axis blockade inhibits regulatory T cell cytotoxicity towards CD8 T cells in the leukemic niche.Nature communications · 2025Article
- Dual targeting of tumoral cells and immune microenvironment by blocking the IL-33/IL1RL1 pathway.Nature communications · 2025Article
- SHP2 inhibition displays efficacy as a monotherapy and in combination with JAK2 inhibition in preclinical models of myeloproliferative neoplasms.American journal of hematology · 2024Article
- SHIP1 deficiency causes inflammation-dependent retardation in skeletal growth.Life science alliance · 2024Article
- Review
- Biological drivers of clinical phenotype in myelofibrosis.Leukemia · 2023Review
- Knowledge mapping and research trends of IL-33 from 2004 to 2022: a bibliometric analysis.Frontiers in immunology · 2023Article
- The role of IL-33/ST2 signaling in the tumor microenvironment and Treg immunotherapy.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- The Role of Neutrophilic Granulocytes in Philadelphia Chromosome Negative Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Adenovirus vector vaccination reprograms pulmonary fibroblastic niches to support protective inflating memory CD8Nature immunology · 2021Article
- Review
- The soluble glycoprotein NMB (GPNMB) produced by macrophages induces cancer stemness and metastasis via CD44 and IL-33.Cellular & molecular immunology · 2021Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
- Fate of Hematopoiesis During Aging. What Do We Really Know, and What are its Implications?Stem cell reviews and reports · 2020Review
- The IL-33 Receptor/ST2 acts as a positive regulator of functional mouse bone marrow hematopoietic stem and progenitor cells.Blood cells, molecules & diseases · 2020Article
- Make killers sweeter: targeting metabolic checkpoints of NK cells.Nature immunology · 2020Article
- Tumour predisposition and cancer syndromes as models to study gene-environment interactions.Nature reviews. Cancer · 2020Review
- Metabolic Vulnerabilities and Epigenetic Dysregulation in Myeloproliferative Neoplasms.Frontiers in immunology · 2020Review
- The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 5 countries.
Funding
Abstract
Myeloproliferative neoplasms (MPNs) are characterized by the clonal expansion of one or more myeloid cell lineage. In most cases, proliferation of the malignant clone is ascribed to defined genetic alterations. MPNs are also associated with aberrant expression and activity of multiple cytokines; however, the mechanisms by which these cytokines contribute to disease pathogenesis are poorly understood. Here, we reveal a non-redundant role for steady-state IL-33 in supporting dysregulated myelopoiesis in a murine model of MPN. Genetic ablation of the IL-33 signaling pathway was sufficient and necessary to restore normal hematopoiesis and abrogate MPN-like disease in animals lacking the inositol phosphatase SHIP. Stromal cell-derived IL-33 stimulated the secretion of cytokines and growth factors by myeloid and non-hematopoietic cells of the BM, resulting in myeloproliferation in SHIP-deficient animals. Additionally, in the transgenic JAK2V617F model, the onset of MPN was delayed in animals lacking IL-33 in radio-resistant cells. In human BM, we detected increased numbers of IL-33-expressing cells, specifically in biopsies from MPN patients. Exogenous IL-33 promoted cytokine production and colony formation by primary CD34+ MPN stem/progenitor cells from patients. Moreover, IL-33 improved the survival of JAK2V617F-positive cell lines. Together, these data indicate a central role for IL-33 signaling in the pathogenesis of MPNs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.