ArticleThe Journal of clinical investigation2024
PD-1H/VISTA mediates immune evasion in acute myeloid leukemia.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
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.
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Who cites it
15 citing papers in PubMed, 14 citations in OpenAlex.
- Immune Checkpoints in Leukaemia as Gatekeepers of Immuno-Modulation.Immunology · 2026Review
- Cancer Immunotherapy: Therapeutic Limitations and Next-Generation Precision Strategies.Immune network · 2026Review
- PD-1 H (VISTA) drives immunosuppressive reprogramming of glioma-associated myeloid cells to promote glioma progression.Journal of translational medicine · 2026Article
- Emerging immune checkpoint targets and combination strategies in blood cancer immunotherapy.Annals of hematology · 2026Review
- The role of immune checkpoints in modulating cancer stem cells anti-tumor immune responses: implications and perspectives in cancer therapy.Journal of experimental & clinical cancer research : CR · 2025Review
- VISTA expressed on tumor cells is regulated by m6A and influences immune microenvironment through STAT3/CCL22 in NSCLC.Journal of translational medicine · 2025Article
- VISTA Alleviates Microglia-Mediated Neuroinflammation After Cerebral Ischemia-Reperfusion Injury via Regulating ACOD1/Itaconic Acid Metabolism.Molecular neurobiology · 2025Article
- Epithelial-Mesenchymal Transition Activates YAP to Drive Malignant Progression and Immune Evasion.Cancers · 2025Article
- Review
- Targeting cell-surface VISTA expression on allospecific naïve T cells promotes tolerance.Blood · 2025Article
- Pathogenesis and inflammaging in myelodysplastic syndrome.Haematologica · 2025Review
- Immune inhibitory receptor agonist therapeutics.Frontiers in immunology · 2025Review
- A pair of promising immune checkpoints PSGL-1 and VISTA from immunotolerance to immunotherapy.Biomarker research · 2024Review
- VISTA-mediated immune evasion in cancer.Experimental & molecular medicine · 2024Review
- VISTA in hematological malignancies: a review of the literature.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
26 authors at 11 institutions in 5 countries.
Funding
Abstract
Acute myeloid leukemia (AML) presents a pressing medical need in that it is largely resistant to standard chemotherapy as well as modern therapeutics, such as targeted therapy and immunotherapy, including anti-programmed cell death protein (anti-PD) therapy. We demonstrate that programmed death-1 homolog (PD-1H), an immune coinhibitory molecule, is highly expressed in blasts from the bone marrow of AML patients, while normal myeloid cell subsets and T cells express PD-1H. In studies employing syngeneic and humanized AML mouse models, overexpression of PD-1H promoted the growth of AML cells, mainly by evading T cell-mediated immune responses. Importantly, ablation of AML cell-surface PD-1H by antibody blockade or genetic knockout significantly inhibited AML progression by promoting T cell activity. In addition, the genetic deletion of PD-1H from host normal myeloid cells inhibited AML progression, and the combination of PD-1H blockade with anti-PD therapy conferred a synergistic antileukemia effect. Our findings provide the basis for PD-1H as a potential therapeutic target for treating human AML.
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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.