ArticleProceedings of the National Academy of Sciences of the United States of America2013
Synergistic inhibition of natural killer cells by the nonsignaling molecule CD94.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Entry into the lytic cycle exposes EBV-infected cells to NK cell killing via upregulation of the MICB ligand for NKG2D and activation of the CD56Frontiers in immunology · 2024Article
- The Role of NK Cells in EBV Infection and Related Diseases: Current Understanding and Hints for Novel Therapies.Cancers · 2023Review
- Disruption of the NKG2A:HLA-E Immune Checkpoint Axis to Enhance NK Cell Activation against Cancer.Vaccines · 2022Review
- Transcriptomic Remodelling of Fetal Endothelial Cells During Establishment of Inflammatory Memory.Frontiers in immunology · 2021Article
- HLA Class I Molecules as Immune Checkpoints for NK Cell Alloreactivity and Anti-Viral Immunity in Kidney Transplantation.Frontiers in immunology · 2021Review
- HLA-E: exploiting pathogen-host interactions for vaccine development.Clinical and experimental immunology · 2019Review
- Conserved and variable natural killer cell receptors: diverse approaches to viral infections.Immunology · 2019Review
- Two to Tango: Co-evolution of Hominid Natural Killer Cell Receptors and MHC.Frontiers in immunology · 2019Review
- Peptide-based materials for cancer immunotherapy.Theranostics · 2019Review
- NKG2A Expression Is NotFrontiers in immunology · 2018Article
- Natural Killer Cell Interactions with Classical and Non-Classical Human Leukocyte Antigen Class I in HIV-1 Infection.Frontiers in immunology · 2017Review
- Article
- MicroRNA profiling of CD3+ CD56+ cytokine-induced killer cells.Scientific reports · 2015Article
- Article
- Effects of Peptide on NK cell-mediated MHC I recognition.Frontiers in immunology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Peptide selectivity is a feature of inhibitory receptors for MHC class I expressed by natural killer (NK) cells. CD94-NKG2A operates in tandem with the polymorphic killer cell Ig-like receptors (KIR) and Ly49 systems to inhibit NK cells. However, the benefits of having two distinct inhibitory receptor-ligand systems are not clear. We show that noninhibitory peptides presented by HLA-E can augment the inhibition of NKG2A(+) NK cells mediated by MHC class I signal peptides through the engagement of CD94 without a signaling partner. Thus, CD94 is a peptide-selective NK cell receptor, and NK cells can be regulated by nonsignaling interactions. We also show that KIR(+) and NKG2A(+) NK cells respond with differing stoichiometries to MHC class I down-regulation. MHC-I-bound peptide functions as a molecular rheostat controlling NK cell function. Selected peptides which in isolation do not inhibit NK cells can have different effects on KIR and NKG2A receptors. Thus, these two inhibitory systems may complement each other by having distinct responses to bound peptide and surface levels of MHC class I.
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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.