ArticleScience (New York, N.Y.)2015
Antitumor immunity. A shed NKG2D ligand that promotes natural killer cell activation and tumor rejection.
Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 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
177 citing papers in PubMed, 244 citations in OpenAlex.
- Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy.Pharmaceutical science advances · 2026Review
- Targeting NKG2D/NKG2DL axis in cancer immunotherapy: mechanisms and therapeutic applications.Journal of translational medicine · 2026Review
- Efficacy of a standardized extract (HemoHIM G) fromFood science and biotechnology · 2025Article
- Intestinal reengineering: Scientific advances in intestinal transplantation.World journal of gastrointestinal surgery · 2025Review
- The Metabolic Regulation of the NKG2D-Positive NK and T Cells and Their Role in Disease Progression.Biomolecules · 2025Review
- Overcoming Immune Therapy Resistance in Cancer Through Innate Immune Reprogramming.International journal of molecular sciences · 2025Review
- Comparative efficacy and safety of PSCA CAR-engineered Vδ1 γδ T cells for immunotherapy of pancreatic cancer.Journal for immunotherapy of cancer · 2025Article
- Peptide-based drugs in immunotherapy: current advances and future prospects.Medical oncology (Northwood, London, England) · 2025Review
- Intranodal injection of neoantigen-bearing engineeredActa pharmaceutica Sinica. B · 2025Article
- 23ME-01473, an Fc Effector-Enhanced Anti-ULBP6/2/5 Antibody, Restores NK Cell-Mediated Antitumor Immunity through NKG2D and FcγRIIIa Activation.Cancer research communications · 2025Article
- Deciphering the mechanistic roles of ADARs in cancer pathogenesis, tumor immune evasion, and drug resistance.Frontiers in immunology · 2025Review
- Designs of NKG2D-based immunotherapeutics for cancer.Frontiers in immunology · 2025Review
- Enhancing natural killer cell anti-tumour activity through macrophage manipulation.Frontiers in immunology · 2025Review
- Colorectal Cancers and Immunotherapy.Cancer treatment and research · 2025Review
- A potential mechanism of tumor immune escape: Regulation and application of soluble natural killer group 2 member D ligands (Review).Oncology reports · 2024Review
- Review
- Arming Vδ2 T Cells with Chimeric Antigen Receptors to Combat Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Review
- Therapeutic effect of small extracellular vesicles from cytokine-induced memory-like natural killer cells on solid tumors.Journal of nanobiotechnology · 2024Article
- Local, Sustained, and Targeted Co-Delivery of MEK Inhibitor and Doxorubicin Inhibits Tumor Progression in E-Cadherin-Positive Breast Cancer.Pharmaceutics · 2024Article
- Microfluidics-assisted fabrication of natural killer cell-laden microgel enhances the therapeutic efficacy for tumor immunotherapy.Materials today. Bio · 2024Article
117 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Immune cells, including natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed immunosurveillance. It is thought that tumor cells evade immunosurveillance by shedding membrane ligands that bind to the NKG2D-activating receptor on NK cells and/or T cells, and desensitize these cells. In contrast, we show that in mice, a shed form of MULT1, a high-affinity NKG2D ligand, causes NK cell activation and tumor rejection. Recombinant soluble MULT1 stimulated tumor rejection in mice. Soluble MULT1 functions, at least in part, by competitively reversing a global desensitization of NK cells imposed by engagement of membrane NKG2D ligands on tumor-associated cells, such as myeloid cells. The results overturn conventional wisdom that soluble ligands are always inhibitory and suggest a new approach for cancer immunotherapy.
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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.