ArticleCancer research2010
Chemotherapy-induced genotoxic stress promotes sensitivity to natural killer cell cytotoxicity by enabling missing-self recognition.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 96 citations in OpenAlex.
- Navigating the immunosuppressive abyss: current hurdles and innovative breakthroughs in neoadjuvant immunotherapy for osteosarcoma.Frontiers in immunology · 2026Review
- Direct immunoactivation by chemotherapeutic drugs in cancer treatment.Advanced therapeutics · 2023Article
- The inhibitory NKR-P1B receptor regulates NK cell-mediated mammary tumor immunosurveillance in mice.Oncoimmunology · 2023Article
- The Role of HDACs in the Response of Cancer Cells to Cellular Stress and the Potential for Therapeutic Intervention.International journal of molecular sciences · 2022Review
- Clr-f expression regulates kidney immune and metabolic homeostasis.Scientific reports · 2022Article
- The Unfolded Protein Response at the Tumor-Immune Interface.Frontiers in immunology · 2022Review
- A Proposed Link Between Acute Thymic Involution and Late Adverse Effects of Chemotherapy.Frontiers in immunology · 2022Article
- Mechanisms, Characteristics, and Treatment of Neuropathic Pain and Peripheral Neuropathy Associated with Dinutuximab in Neuroblastoma Patients.International journal of molecular sciences · 2021Review
- Natural Killer Cells and Anti-Cancer Therapies: Reciprocal Effects on Immune Function and Therapeutic Response.Cancers · 2021Review
- Clinical Data on Immunotherapy in Breast Cancer.Breast care (Basel, Switzerland) · 2020Review
- DNT Cell-based Immunotherapy: Progress and Applications.Journal of Cancer · 2020Review
- Cytotoxicity of Donor Natural Killer Cells to Allo-Reactive T Cells Are Related With Acute Graft-vs.-Host-Disease Following Allogeneic Stem Cell Transplantation.Frontiers in immunology · 2020Article
- Cytotoxic Immunity in Peripheral Nerve Injury and Pain.Frontiers in neuroscience · 2020Review
- Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b.Journal of virology · 2019Article
- Production of recombinant soluble dimeric C-type lectin-like receptors of rat natural killer cells.Scientific reports · 2019Article
- Killers 2.0: NK cell therapies at the forefront of cancer control.The Journal of clinical investigation · 2019Review
- Naturally Killing the Silent Killer: NK Cell-Based Immunotherapy for Ovarian Cancer.Frontiers in immunology · 2019Review
- NKG2D/NKG2-Ligand Pathway Offers New Opportunities in Cancer Treatment.Frontiers in immunology · 2019Review
- Recognition of host Clr-b by the inhibitory NKR-P1B receptor provides a basis for missing-self recognition.Nature communications · 2018Article
- Challenges of NK cell-based immunotherapy in the new era.Frontiers of medicine · 2018Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Natural killer (NK) cells can recognize and kill tumor cells lacking "self" markers, such as class I MHC, but the basis for this recognition is not completely understood. NKR-P1 receptors are members of the C-type lectin-related NK receptor superfamily that are conserved from rodents to humans. Identification of Clr ligands for the NKR-P1 receptors has facilitated functional analysis of MHC-independent target cell recognition by NK cells. One receptor-ligand pair, NKR-P1B:Clr-b, can mediate "missing-self" recognition of tumor and infected cells, but the role of this axis in sensing stressed cells remains unknown. Here, we show that Clr-b is rapidly downregulated in cells undergoing genotoxic and cellular stress at the level of both RNA and surface protein. Stress-mediated loss of Clr-b on leukemia cells enhanced cytotoxicity mediated by NKR-P1B(+) NK cells. Notably, Clr-b downregulation was coordinated functionally with stress-mediated upregulation of NKG2D ligands (but not class I MHC). Our findings highlight a unique role for the MHC-independent NKR-P1B:Clr-b missing-self axis in recognition of stressed cells, and provide evidence of two independent levels of Clr-b regulation in stressed cells.
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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.