ArticleRheumatology (Oxford, England)2013
The arthritis-associated HLA-B*27:05 allele forms more cell surface B27 dimer and free heavy chain ligands for KIR3DL2 than HLA-B*27:09.
Article in Rheumatology (Oxford, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 61 citations in OpenAlex.
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- Inhibitory KIRs decrease HLA class II-mediated protection in Type 1 Diabetes.PLoS genetics · 2024Article
- PepCARES: A Comprehensive Advanced Refinement and Evaluation System for Peptide Design and Affinity Screening.ACS omega · 2024Article
- Cell Surface B2m-Free Human Leukocyte Antigen (HLA) Monomers and Dimers: Are They Neo-HLA Class and Proto-HLA?Biomolecules · 2023Review
- EULAR study group on 'MHC-I-opathy': identifying disease-overarching mechanisms across disciplines and borders.Annals of the rheumatic diseases · 2023Review
- Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023Review
- Population Genetics and Signatures of Selection in Early Neolithic European Farmers.Molecular biology and evolution · 2022Article
- Spondyloarthritides: Theories and beyond.Frontiers in pediatrics · 2022Review
- Joint together: The etiology and pathogenesis of ankylosing spondylitis.Frontiers in immunology · 2022Review
- Aberrant antigen processing and presentation: Key pathogenic factors leading to immune activation in Ankylosing spondylitis.Seminars in immunopathology · 2021Review
- Spondyloarthritis and the Human Leukocyte Antigen (HLA)-BFrontiers in immunology · 2021Review
- HLA-B27 association of autoimmune encephalitis induced by PD-L1 inhibitor.Annals of clinical and translational neurology · 2020Article
- Understanding the Pathogenesis of Spondyloarthritis.Biomolecules · 2020Review
- Two Lineages ofJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Allelic association with ankylosing spondylitis fails to correlate with human leukocyte antigen B27 homodimer formation.The Journal of biological chemistry · 2019Article
- HLA associations in inflammatory arthritis: emerging mechanisms and clinical implications.Nature reviews. Rheumatology · 2019Review
- Allele-specific Alterations in the Peptidome Underlie the Joint Association of HLA-A*29:02 and Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) with Birdshot Chorioretinopathy.Molecular & cellular proteomics : MCP · 2018Article
- Expression and Metabolomic Profiling in Axial Spondyloarthritis.Current rheumatology reports · 2018Review
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24 authors at 1 institution in 1 country.
Funding
Abstract
objectivesHLA-B*27:05 is associated with AS whereas HLA-B*27:09 is not associated. We hypothesized that different interactions with KIR immune receptors could contribute to the difference in disease association between HLA-B*27:05 and HLAB*27:09. Thus, the objective of this study was to compare the formation of β2m-free heavy chain (FHC) including B27 dimers (B272) by HLA-B*27:05 and HLA-B*27:09 and their binding to KIR immunoreceptors.
methodsWe studied the formation of HLA-B*27:05 and HLA-B*27:09 heterotrimers and FHC forms including dimers in vitro and in transfected cells. We investigated HLA-B*27:05 and HLA-B*27:09 binding to KIR3DL1, KIR3DL2 and LILRB2 by FACS staining with class I tetramers and by quantifying interactions with KIR3DL2CD3ε-reporter cells and KIR3DL2-expressing NK cells. We also measured KIR expression on peripheral blood NK and CD4 T cells from 18 HLA-B*27:05 AS patients, 8 HLA-B27 negative and 12 HLA-B*27:05+ and HLA-B*27:09+ healthy controls by FACS staining.
resultsHLA-B*27:09 formed less B27₂ and FHC than HLA-B*27:05. HLA-B*27:05-expressing cells stimulated KIR3DL2CD3ε-reporter T cells more effectively. Cells expressing HLA-B*27:05 promoted KIR3DL2+ NK cell survival more strongly than HLA-B*27:09. HLA-B*27:05 and HLA-B*27:09 dimer tetramers stained KIR3DL1, KIR3DL2 and LILRB2 equivalently. Increased proportions of NK and CD4 T cells expressed KIR3DL2 in HLA-B*27:05+ AS patients compared with HLA-B*27:05+, HLA-B*27:09+ and HLA-B27- healthy controls.
conclusionDifferences in the formation of FHC ligands for KIR3DL2 by HLA-B*27:05 and HLA-B*27:09 could contribute to the differential association of these alleles with AS.
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