ArticleCancer immunology, immunotherapy : CII2023
Invariant NKT cells metabolically adapt to the acute myeloid leukaemia environment.
Article in Cancer immunology, immunotherapy : CII, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 16 citations in OpenAlex.
- Recent advances of cell therapies for AML/MDS: exploring the therapeutic potential of innate immune cells in AML/MDS.International journal of hematology · 2026Review
- BCAAs and related metabolic enzymes: partners in crime driving tumor development.Frontiers in cell and developmental biology · 2026Review
- T-Cell Responses and T-Cell-Based Therapy in Acute Myeloid Leukemia.Current medical science · 2025Review
- Amino acid metabolic reprogramming drives pathogenesis and therapy in hematologic malignancies.Discover oncology · 2025Review
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- Interplay between innate-like T-cells and microRNAs in cancer immunity.Discover oncology · 2025Review
- NKT cells-a generalist in disease treatment and a new key to unlock immunotherapy.Immunotherapy · 2025Review
- SAA1 Protein: A Potential Biomarker for Acute Myeloid Leukemia.Biomedicines · 2025Article
- BCAA metabolism in cancer progression and therapy resistance: The balance between fuel and cell signaling.Frontiers in pharmacology · 2025Review
- Review
- Natural Killer T Cell Diversity and Immunotherapy.Cancers · 2023Review
- Beyond αβ T cells: NK, iNKT, and γδT cell biology in leukemic patients and potential for off-the-shelf adoptive cell therapies for AML.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 1 country.
Funding
Abstract
Acute myeloid leukaemia (AML) creates an immunosuppressive environment to conventional T cells through Arginase 2 (ARG2)-induced arginine depletion. We identify that AML blasts release the acute phase protein serum amyloid A (SAA), which acts in an autocrine manner to upregulate ARG2 expression and activity, and promote AML blast viability. Following in vitro cross-talk invariant natural killer T (iNKT) cells become activated, upregulate mitochondrial capacity, and release IFN-γ. iNKT retain their ability to proliferate and be activated despite the low arginine AML environment, due to the upregulation of Large Neutral Amino Acid Transporter-1 (LAT-1) and Argininosuccinate Synthetase 1 (ASS)-dependent amino acid pathways, resulting in AML cell death. T cell proliferation is restored in vitro and in vivo. The capacity of iNKT cells to restore antigen-specific T cell immunity was similarly demonstrated against myeloid-derived suppressor cells (MDSCs) in wild-type and Jα18
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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.