ArticleNature communications2018
Recognition of host Clr-b by the inhibitory NKR-P1B receptor provides a basis for missing-self recognition.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 23 citations in OpenAlex.
- Translational Insights into NK Immunophenotyping: Comparative Surface Marker Analysis and Circulating Immune Cell Profiling in Cancer Immunotherapy.International journal of molecular sciences · 2025Review
- MICBG406A polymorphism reduces risk of mechanical ventilation and death during viral acute lung injury.JCI insight · 2025Article
- Recognition of Self and Viral Ligands by NK Cell Receptors.Immunological reviews · 2025Review
- Observational
- The diverse roles of C-type lectin-like receptors in immunity.Frontiers in immunology · 2023Review
- Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death.Nature communications · 2022Article
- Structure of the human NK cell NKR-P1:LLT1 receptor:ligand complex reveals clustering in the immune synapse.Nature communications · 2022Article
- Increased expression of TIGIT and KLRG1 correlates with impaired CD56Virology journal · 2022Article
- Clr-f expression regulates kidney immune and metabolic homeostasis.Scientific reports · 2022Article
- Mouse Ocilrp2/Clec2i negatively regulates LPS-mediated IL-6 production by blocking Dap12-Syk interaction in macrophage.Frontiers in immunology · 2022Article
- Natural Killer Cells and Anti-Cancer Therapies: Reciprocal Effects on Immune Function and Therapeutic Response.Cancers · 2021Review
- Natural killer cells in cancer biology and therapy.Molecular cancer · 2020Review
- Modulation of innate and adaptive immunity by cytomegaloviruses.Nature reviews. Immunology · 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
- Structural basis for the recognition of nectin-like protein-5 by the human-activating immune receptor, DNAM-1.The Journal of biological chemistry · 2019Article
- Oligomeric Architecture of Mouse Activating Nkrp1 Receptors on Living Cells.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
The interaction between natural killer (NK) cell inhibitory receptors and their cognate ligands constitutes a key mechanism by which healthy tissues are protected from NK cell-mediated lysis. However, self-ligand recognition remains poorly understood within the prototypical NKR-P1 receptor family. Here we report the structure of the inhibitory NKR-P1B receptor bound to its cognate host ligand, Clr-b. NKR-P1B and Clr-b interact via a head-to-head docking mode through an interface that includes a large array of polar interactions. NKR-P1B:Clr-b recognition is extremely sensitive to mutations at the heterodimeric interface, with most mutations severely impacting both Clr-b binding and NKR-P1B receptor function to implicate a low affinity interaction. Within the structure, two NKR-P1B:Clr-b complexes are cross-linked by a non-classic NKR-P1B homodimer, and the disruption of homodimer formation abrogates Clr-b recognition. These data provide an insight into a fundamental missing-self recognition system and suggest an avidity-based mechanism underpins NKR-P1B receptor function.
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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.