ArticleNature immunology2022
ILC1s control leukemia stem cell fate and limit development of AML.
Article in Nature immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Trial
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- A Link Between Allergy and Hematological Malignancies? Focus on Possible Mechanisms and the Potential Role of Biological Therapies.Clinical and translational allergy · 2026Review
- Human type-1 innate lymphoid cells control leukemia stem cell differentiation and limit acute myeloid leukemia development.Nature communications · 2026Article
- Targeting leukemic stem cell biomechanics suppresses stemness and enhances NK cell-mediated immunotherapy.Nature communications · 2025Article
- Emerging strategies and novel therapeutic targets in acute myeloid leukemia: current advances and future directions.Biomarker research · 2025Review
- Emerging combined CAR-NK cell therapies in cancer treatment: Finding a dancing partner.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- NKp46 enhances type 1 innate lymphoid cell proliferation and function and anti-acute myeloid leukemia activity.Nature communications · 2025Article
- Immunotherapy for high-grade endometrial stromal sarcoma: a narrative review bridging molecular insights to clinical translation.Frontiers in immunology · 2025Review
- Advances in preclinical and clinical studies of oncolytic virus combination therapy.Frontiers in oncology · 2025Review
- GPR34 is a metabolic immune checkpoint for ILC1-mediated antitumor immunity.Nature immunology · 2024Article
- Article
- The paradoxical role of cytokines and chemokines at the tumor microenvironment: a comprehensive review.European journal of medical research · 2024Review
- Article
- Emerging roles of type 1 innate lymphoid cells in tumour pathogenesis and cancer immunotherapy.Exploration of targeted anti-tumor therapy · 2024Review
- Emerging and Future Targeted Therapies for Pediatric Acute Myeloid Leukemia: Targeting the Leukemia Stem Cells.Biomedicines · 2023Review
- Review
- FOXO1 orchestrates the intestinal homeostasis via neuronal signaling in group 3 innate lymphoid cells.The Journal of experimental medicine · 2023Article
- IL-18 and VEGF-A trigger type 2 innate lymphoid cell accumulation and pro-tumoral function in chronic myeloid leukemia.Haematologica · 2023Article
- Targeting Potential of Innate Lymphoid Cells in Melanoma and Other Cancers.Pharmaceutics · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Type I innate lymphoid cells (ILC1s) are critical regulators of inflammation and immunity in mammalian tissues. However, their function in cancer is mostly undefined. Here, we show that a high density of ILC1s induces leukemia stem cell (LSC) apoptosis in mice. At a lower density, ILC1s prevent LSCs from differentiating into leukemia progenitors and promote their differentiation into non-leukemic cells, thus blocking the production of terminal myeloid blasts. All of these effects, which require ILC1s to produce interferon-γ after cell-cell contact with LSCs, converge to suppress leukemogenesis in vivo. Conversely, the antileukemia potential of ILC1s wanes when JAK-STAT or PI3K-AKT signaling is inhibited. The relevant antileukemic properties of ILC1s are also functional in healthy individuals and impaired in individuals with acute myeloid leukemia (AML). Collectively, these findings identify ILC1s as anticancer immune cells that might be suitable for AML immunotherapy and provide a potential strategy to treat AML and prevent relapse of the disease.
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What OpenQuestion holds
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.