ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Polymorphic sites away from the Bw4 epitope that affect interaction of Bw4+ HLA-B with KIR3DL1.
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 44 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Behçet's Disease: A Comprehensive Review on the Role ofInternational journal of molecular sciences · 2023Pooled it
- High resolution class I HLA-A, -B, and -C diversity in Eastern and Southern African populations.Scientific reports · 2025Article
- The complex HLA-E-nonapeptide in Behçet disease.Frontiers in immunology · 2023Article
- The HLA-G Immune Checkpoint Plays a Pivotal Role in the Regulation of Immune Response in Autoimmune Diseases.International journal of molecular sciences · 2021Review
- The Role of Natural Killer Cells in Autoimmune Diseases.Frontiers in immunology · 2021Review
- Article
- Pathogenesis of Non-Infectious Uveitis Elucidated by Recent Genetic Findings.Frontiers in immunology · 2021Review
- Epistatic interactions between killer immunoglobulin-like receptors and human leukocyte antigen ligands are associated with ankylosing spondylitis.PLoS genetics · 2020Article
- In vitro education of human natural killer cells by KIR3DL1.Life science alliance · 2019Article
- KIR3DL1/S1 Allotypes Contribute Differentially to the Development of Behçet Disease.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- The association analysis between HLA-A*26 and Behçet's disease.Scientific reports · 2019Article
- Two to Tango: Co-evolution of Hominid Natural Killer Cell Receptors and MHC.Frontiers in immunology · 2019Review
- Association of Functional Polymorphisms of KIR3DL1/DS1 With Behçet's Disease.Frontiers in immunology · 2019Article
- Deciphering the killer-cell immunoglobulin-like receptor system at super-resolution for natural killer and T-cell biology.Immunology · 2017Review
- 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
- Article
- 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
- Article
- The immunogenetics of Behçet's disease: A comprehensive review.Journal of autoimmunity · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
KIR3DL1 is a polymorphic, inhibitory NK cell receptor specific for the Bw4 epitope carried by subsets of HLA-A and HLA-B allotypes. The Bw4 epitope of HLA-B*5101 and HLA-B*1513 is determined by the NIALR sequence motif at positions 77, 80, 81, 82, and 83 in the alpha(1) helix. Mutation of these positions to the residues present in the alternative and nonfunctional Bw6 motif showed that the functional activity of the Bw4 epitopes of B*5101 and B*1513 is retained after substitution at positions 77, 80, and 81, but lost after substitution of position 83. Mutation of leucine to arginine at position 82 led to loss of function for B*5101 but not for B*1513. Further mutagenesis, in which B*1513 residues were replaced by their B*5101 counterparts, showed that polymorphisms in all three extracellular domains contribute to this functional difference. Prominent were positions 67 in the alpha(1) domain, 116 in the alpha(2) domain, and 194 in the alpha(3) domain. Lesser contributions were made by additional positions in the alpha(2) domain. These positions are not part of the Bw4 epitope and include residues shaping the B and F pockets that determine the sequence and conformation of the peptides bound by HLA class I molecules. This analysis shows how polymorphism at sites throughout the HLA class I molecule can influence the interaction of the Bw4 epitope with KIR3DL1. This influence is likely mediated by changes in the peptides bound, which alter the conformation of the Bw4 epitope.
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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.