ArticleOncotarget2015
Differential expression and biochemical activity of the immune receptor Tim-3 in healthy and malignant human myeloid cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026Review
- Ligand-receptor interactions of V-domain Ig-containing suppressor of T cell activation and programmed death-1 suppress the anticancer activities of T cells.Immuno-oncology technology · 2025Article
- Galectin-9 induces IL-1β production as a key inflammatory cytokine in the acute myeloid leukemia cell line (U937).Research in pharmaceutical sciences · 2025Article
- Galectin-9, a pro-survival factor inducing immunosuppression, leukemic cell transformation and expansion.Molecular biology reports · 2024Review
- Article
- Multiple myeloma and the potential of new checkpoint inhibitors for immunotherapy.Therapeutic advances in vaccines and immunotherapy · 2024Review
- The role of bone marrow microenvironment (BMM) cells in acute myeloid leukemia (AML) progression: immune checkpoints, metabolic checkpoints, and signaling pathways.Cell communication and signaling : CCS · 2023Review
- Checkpoint Inhibitors in Acute Myeloid Leukemia.Biomedicines · 2023Review
- Review
- TIM-3/Gal-9 interaction affects glucose and lipid metabolism in acute myeloid leukemia cell lines.Frontiers in immunology · 2023Article
- T lymphocytes induce human cancer cells derived from solid malignant tumors to secrete galectin-9 which facilitates immunosuppression in cooperation with other immune checkpoint proteins.Journal for immunotherapy of cancer · 2023Article
- New Checkpoint Inhibitors on the Road: Targeting TIM-3 in Solid Tumors.Current oncology reports · 2022Review
- Expression of the Immune Checkpoint Protein VISTA Is Differentially Regulated by the TGF-β1 - Smad3 Signaling Pathway in Rapidly Proliferating Human Cells and T Lymphocytes.Frontiers in medicine · 2022Article
- DNAM-1/CD226 is functionally expressed on acute myeloid leukemia (AML) cells and is associated with favorable prognosis.Scientific reports · 2021Article
- TIM-3 in normal and malignant hematopoiesis: Structure, function, and signaling pathways.Cancer science · 2021Review
- Expression of immune check point gene TIM-3 in patients newly diagnosed with acute myeloid leukemia: Significance and impact on outcome.Oncology letters · 2021Article
- Advanced Nanotechnology for Enhancing Immune Checkpoint Blockade Therapy.Nanomaterials (Basel, Switzerland) · 2021Review
- One Stone, Two Birds: The Roles of Tim-3 in Acute Myeloid Leukemia.Frontiers in immunology · 2021Review
- High Mobility Group Box 1 (HMGB1) Induces Toll-Like Receptor 4-Mediated Production of the Immunosuppressive Protein Galectin-9 in Human Cancer Cells.Frontiers in immunology · 2021Article
- TIM-3 in Leukemia; Immune Response and Beyond.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The T cell immunoglobulin and mucin domain 3 (Tim-3) is a plasma membrane-associated receptor which is involved in a variety of biological responses in human immune cells. It is highly expressed in most acute myeloid leukaemia (AML) cells and therefore may serve as a possible target for AML therapy. However, its biochemical activities in primary human AML cells remain unclear. We therefore analysed the total expression and surface presence of the Tim-3 receptor in primary human AML blasts and healthy primary human leukocytes isolated from human blood. We found that Tim-3 expression was significantly higher in primary AML cells compared to primary healthy leukocytes. Tim-3 receptor molecules were distributed largely on the surface of primary AML cells, whereas in healthy leukocytes Tim-3 protein was mainly expressed intracellularly. In primary human AML blasts, both Tim-3 agonistic antibody and galectin-9 (a Tim-3 natural ligand) significantly upregulated mTOR pathway activity. This was in line with increased accumulation of hypoxia-inducible factor 1 alpha (HIF-1α) and secretion of VEGF and TNF-α. Similar results were obtained in primary human healthy leukocytes. Importantly, in both types of primary cells, Tim-3-mediated effects were compared with those induced by lipopolysaccharide (LPS) and stem cell factor (SCF). Tim-3 induced comparatively moderate responses in both AML cells and healthy leukocytes. However, Tim-3, like LPS, mediated the release of both TNF-α and VEGF, while SCF induced mostly VEGF secretion and did not upregulate TNF-α release.
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