ArticleBlood2023
Therapeutic activity of GARP:TGF-β1 blockade in murine primary myelofibrosis.
Article in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia.Blood · 2026Article
- Platelets as localized conduits of TGF-β1 in the tumor microenvironment: implications for cancer progression and therapy.Human cell · 2026Review
- CTHRC1 drives megakaryocyte-mediated immunotherapy resistance in esophageal squamous cell carcinoma via the integrin αIIbβ3/Rap1 pathway and is targetable by mRNA vaccination.Molecular cancer · 2026Article
- Hematopoietic Niche Hijacking in Bone Metastases: Roles of Megakaryocytes, Erythroid Lineage Cells, and Perivascular Stromal Subsets.Biomedicines · 2026Review
- Cancer cells metastasize in several types of cancer via two distinct routes, probably based on mechanical signals.Frontiers in cell and developmental biology · 2026Review
- GARP-expressing Tregs as a source of immunosuppressive TGF-β1 in human tumors.Cancer immunology, immunotherapy : CII · 2025Article
- Platelets in cancer and immunotherapy: functional dynamics and therapeutic opportunities.Experimental hematology & oncology · 2025Review
- Targeted Therapies in Myelofibrosis: Present Landscape, Ongoing Studies, and Future Perspectives.American journal of hematology · 2025Review
- TGF-β inhibition restores hematopoiesis and immune balance via bone marrow EPCs in aplastic anemia.Experimental & molecular medicine · 2025Article
- Different inflammatory, fibrotic, and immunological signatures between pre-fibrotic and overt primary myelofibrosis.Haematologica · 2025Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- Biodegradable and injectable curcumin-loaded hydrogel for the prevention of postoperative intrauterine adhesion.Frontiers in bioengineering and biotechnology · 2025Article
- Amorphous curcumin-based hydrogels to reduce the incidence of post-surgical intrauterine adhesions.Regenerative biomaterials · 2024Article
- Endothelial LATS2 is a suppressor of bone marrow fibrosis.Nature cardiovascular research · 2024Article
- Article
- GARP on hepatic stellate cells is essential for the development of liver fibrosis.Journal of hepatology · 2023Article
- Recent advances in therapies for primary myelofibrosis.Faculty reviews · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by the clonal expansion of myeloid cells, notably megakaryocytes (MKs), and an aberrant cytokine production leading to bone marrow (BM) fibrosis and insufficiency. Current treatment options are limited. TGF-β1, a profibrotic and immunosuppressive cytokine, is involved in PMF pathogenesis. While all cell types secrete inactive, latent TGF-β1, only a few activate the cytokine via cell type-specific mechanisms. The cellular source of the active TGF-β1 implicated in PMF is not known. Transmembrane protein GARP binds and activates latent TGF-β1 on the surface of regulatory T lymphocytes (Tregs) and MKs or platelets. Here, we found an increased expression of GARP in the BM and spleen of mice with PMF and tested the therapeutic potential of a monoclonal antibody (mAb) that blocks TGF-β1 activation by GARP-expressing cells. GARP:TGF-β1 blockade reduced not only fibrosis but also the clonal expansion of transformed cells. Using mice carrying a genetic deletion of Garp in either Tregs or MKs, we found that the therapeutic effects of GARP:TGF-β1 blockade in PMF imply targeting GARP on Tregs. These therapeutic effects, accompanied by increased IFN-γ signals in the spleen, were lost upon CD8 T-cell depletion. Our results suggest that the selective blockade of TGF-β1 activation by GARP-expressing Tregs increases a CD8 T-cell-mediated immune reaction that limits transformed cell expansion, providing a novel approach that could be tested to treat patients with myeloproliferative neoplasms.
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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.