ArticleJournal of immunology (Baltimore, Md. : 1950)2015
The interaction of KIR3DL1*001 with HLA class I molecules is dependent upon molecular microarchitecture within the Bw4 epitope.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Methods for Probing NK Cell Surveillance of Antigen Presentation.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Article
- Rhesus Macaque Killer Cell Ig-like Receptor Domain 0 Glycans Impact Surface Expression and Ligand Specificity.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Article
- Multi-epitope peptide vaccines targeting dengue virus serotype 2 created via immunoinformatic analysis.Scientific reports · 2024Article
- Mapping the interplay between NK cells and HIV: therapeutic implications.Journal of leukocyte biology · 2023Review
- KIR Allelic Variation and the Remission of Atopic Dermatitis Over Time.ImmunoHorizons · 2023Article
- NK cell education: Physiological and pathological influences.Frontiers in immunology · 2023Review
- Association of KIR Genes and MHC Class I Ligands with Atopic Dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- HLA Class I Polymorphisms Influencing Both Peptide Binding and KIR Interactions Are Associated with Remission among Children with Atopic Dermatitis: A Longitudinal Study.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The molecular basis of how buried human leukocyte antigen polymorphism modulates natural killer cell function.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Alterations in the HLA-B*57:01 Immunopeptidome by Flucloxacillin and Immunogenicity of Drug-Haptenated Peptides.Frontiers in immunology · 2020Article
- KIR3DL1/S1 Allotypes Contribute Differentially to the Development of Behçet Disease.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Two to Tango: Co-evolution of Hominid Natural Killer Cell Receptors and MHC.Frontiers in immunology · 2019Review
- KIR2DL2 combined with HLA-C1 confers risk of hepatitis C virus-related hepatocellular carcinoma in younger patients.Oncotarget · 2018Article
- Adverse drug reactions triggered by the common HLA-B*57:01 variant: virtual screening of DrugBank using 3D molecular docking.Journal of cheminformatics · 2018Article
- HLA-Bw4-I-80 Isoform Differentially Influences Clinical Outcome As Compared to HLA-Bw4-T-80 and HLA-A-Bw4 Isoforms in Rituximab or Dinutuximab-Based Cancer Immunotherapy.Frontiers in immunology · 2017Article
- Killer cell immunoglobulin-like receptor 3DL1 polymorphism defines distinct hierarchies of HLA class I recognition.The Journal of experimental medicine · 2016Article
- The evolution of natural killer cell receptors.Immunogenetics · 2016Review
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Authors and funding
13 authors at 7 institutions in 4 countries.
Funding
Abstract
The killer cell Ig-like receptor 3DL1 (KIR3DL1) inhibits activation of NK cells upon interaction with HLA class I molecules such as HLA-B*57:01, which contains the Bw4 epitope spanning residues 77-83 (e.g., NLRIALR), and not with HLA allomorphs that possess the Bw6 motif (e.g., HLA-B*08:01), which differ at residues 77, 80, 81, 82, and 83. Although Bw4 residues Ile(80) and Arg(83) directly interact with KIR3DL1*001, their precise role in determining KIR3DL1-HLA-Bw4 specificity remains unclear. Recognition of HLA-B*57:01 by either KIR3DL1(+) NK cells or the NK cell line YTS transfected with KIR3DL1*001 was impaired by mutation of residues 80 and 83 of HLA-B*57:01 to the corresponding amino acids within the Bw6 motif. Conversely, the simultaneous introduction of three Bw4 residues at positions 80, 82, and 83 into HLA-B*08:01 conferred an interaction with KIR3DL1*001. Structural analysis of HLA-B*57:01, HLA-B*08:01, and mutants of each bearing substitutions at positions 80 and 83 revealed that Ile(80) and Arg(83) within the Bw4 motif constrain the conformation of Glu(76), primarily through a salt bridge between Arg(83) and Glu(76). This salt bridge was absent in HLA-Bw6 molecules as well as position 83 mutants of HLA-B*57:01. Mutation of the Bw4 residue Ile(80) also disrupted this salt bridge, providing further insight into the role that position 80 plays in mediating KIR3DL1 recognition. Thus, the strict conformation of HLA-Bw4 allotypes, held in place by the Glu(76)-Arg(83) interaction, facilitates KIR3DL1 binding, whereas Bw6 allotypes present a platform on the α1 helix that is less permissive for KIR3DL1 binding.
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