ArticleOncoimmunology2016
The immune receptor Tim-3 acts as a trafficker in a Tim-3/galectin-9 autocrine loop in human myeloid leukemia cells.
Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- Spatially resolved transcriptomics identifies intercellular signaling post-ischemic stroke that controls neural stem cell proliferation.Stem cell reports · 2026Article
- TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026Review
- From monoclonals to bispecific T cell engagers: the evolving antibody-based therapy landscape in acute myeloid leukemia.Frontiers in immunology · 2026Review
- Galectin-9-An Emerging Glyco-Immune Checkpoint Target for Cancer Therapy.International journal of molecular sciences · 2025Review
- Wuhan strain of SARS-CoV-2 triggers activation of immune evasion machinery similar to the one operated by cancer cells.Frontiers in immunology · 2025Article
- Galectins-1, -3 and -9 in leukemia: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- Dual-targeting CD33/CD123 NANOBODY T-cell engager with potent anti-AML activity and good safety profile.Blood advances · 2024Article
- Galectin-9, a pro-survival factor inducing immunosuppression, leukemic cell transformation and expansion.Molecular biology reports · 2024Review
- TIM-3/Galectin-9 interaction and glutamine metabolism in AML cell lines, HL-60 and THP-1.BMC cancer · 2024Article
- NK cell-based tumor immunotherapy.Bioactive materials · 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
- Immunotherapy in leukaemia.Acta biochimica et biophysica Sinica · 2023Review
- Chimera and Tandem-Repeat Type Galectins: The New Targets for Cancer Immunotherapy.Biomolecules · 2023Review
- TIM-3 signaling hijacks the canonical Wnt/β-catenin pathway to maintain cancer stemness in acute myeloid leukemia.Blood advances · 2023Article
- Antibody therapies for the treatment of acute myeloid leukemia: exploring current and emerging therapeutic targets.Expert opinion on investigational drugs · 2023Review
- Expression of Galectin-9-related immune checkpoint receptors in B-cell acute lymphoblastic leukemia.Iranian journal of basic medical sciences · 2023Article
- A potential area of use for immune checkpoint inhibitors: Targeting bone marrow microenvironment in acute myeloid leukemia.Frontiers in immunology · 2023Review
- 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
- L-Kynurenine participates in cancer immune evasion by downregulating hypoxic signaling in T lymphocytes.Oncoimmunology · 2023Article
- Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune receptor Tim-3 is often highly expressed in human acute myeloid leukemia (AML) cells where it acts as a growth factor and inflammatory receptor. Recently, it has been demonstrated that Tim-3 forms an autocrine loop with its natural ligand galectin-9 in human AML cells. However, the pathophysiological functions of Tim-3 in human AML cells remain unclear. Here, we report for the first time that Tim-3 is required for galectin-9 secretion in human AML cells. However, this effect is cell-type specific and was found so far to be applicable only to myeloid (and not, for example, lymphoid) leukemia cells. We concluded that AML cells might use Tim-3 as a trafficker for the secretion of galectin-9 which can then be possibly used to impair the anticancer activities of cytotoxic T cells and natural killer (NK) cells.
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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.