ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Blocking NK cell inhibitory self-recognition promotes antibody-dependent cellular cytotoxicity in a model of anti-lymphoma therapy.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
106 citing papers in PubMed, 169 citations in OpenAlex.
- Improving selection of patients with metastatic colorectal cancer to benefit from cetuximab based on KIR genotypes.Journal for immunotherapy of cancer · 2021Trial
- Phase 1/2 trial of SARS-CoV-2 vaccine ChAdOx1 nCoV-19 with a booster dose induces multifunctional antibody responses.Nature medicine · 2021Trial
- The membrane distal domain of CD16a allosterically regulates NK cell ADCC.bioRxiv : the preprint server for biology · 2026Article
- Inhibitory NK receptor expression associates with altered antimalarial function of γδ T cells.PLoS pathogens · 2026Article
- Quantitative measures of humanPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Immune Modulation Through KIR-HLA Interactions Influences Cetuximab Efficacy in Colorectal Cancer.International journal of molecular sciences · 2025Article
- 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
- The FcγRIIIA (CD16) L48-H/R Polymorphism Enhances NK Cell-Mediated Antibody-Dependent Cellular Cytotoxicity by Promoting Serial Killing.Cancer immunology research · 2025Article
- Prospects for potential therapy targeting immune‑associated factors in endometriosis (Review).Molecular medicine reports · 2025Review
- Article
- Imaging-Based Efficacy Evaluation of Cancer Immunotherapy in Engineered Tumor Platforms and Tumor Organoids.Advanced healthcare materials · 2024Review
- NK Cytotoxicity Mediated by NK-92 Cell Lines Expressing Combinations of Two Allelic Variants forAntibodies (Basel, Switzerland) · 2024Article
- Evolution of the clinical-stage hyperactive TcBuster transposase as a platform for robust non-viral production of adoptive cellular therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Distinct CD16a features on human NK cells observed by flow cytometry correlate with increased ADCC.Scientific reports · 2024Article
- iPSC-derived natural killer cells expressing the FcγR fusion CD64/16A can be armed with antibodies for multitumor antigen targeting.Journal for immunotherapy of cancer · 2023Article
- Ablation of SYK Kinase from Expanded Primary Human NK Cells via CRISPR/Cas9 Enhances Cytotoxicity and Cytokine Production.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Evaluation of KIR3DL1/KIR3DS1 allelic polymorphisms in Kenyan children with endemic Burkitt lymphoma.PloS one · 2023Article
- Gene-edited and CAR-NK cells: Opportunities and challenges with engineering of NK cells for immunotherapy.Molecular therapy oncolytics · 2022Review
- The multitargeted receptor tyrosine kinase inhibitor sunitinib induces resistance of HER2 positive breast cancer cells to trastuzumab-mediated ADCC.Cancer immunology, immunotherapy : CII · 2022Article
- Harnessing natural killer cells for cancer immunotherapy: dispatching the first responders.Nature reviews. Drug discovery · 2022Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Human NK cells lyse Ab-coated target cells through the process of Ab-dependent cellular cytotoxicity (ADCC). Improving ADCC responses is desirable because it is thought to be an important antitumor mechanism for some Abs. NK cell inhibitory receptors, such as killer cell Ig-like receptors, engage with MHC class I molecules on self-cells to block NK cell activation. Accordingly, we enhanced ADCC responses by blocking NK cell inhibitory receptors, thus perturbing induction of the self-recognition signal. In a cell line model of anti-lymphoma therapy, the combination of rituximab with an Ab that blocks inhibitory self-recognition yielded increased NK cell-mediated target cell lysis when compared with rituximab alone. To validate this proof-of-concept, we then used a more representative approach in which an individual's fresh primary NK cells encountered autologous, EBV-transformed B cells. In this system, rituximab and a combination of Abs that block NK cell inhibitory receptors yielded improved NK cell-mediated lysis over rituximab alone. The results show, for the first time, that disruption of inhibitory self-recognition can efficiently promote ADCC in a human model, applying an autologous system in which physiologic checkpoints are in place. This method provides an alternative approach to potentiate the therapeutic benefit of antitumor Abs that mediate ADCC.
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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.