ArticlePLoS genetics2020
Epistatic interactions between killer immunoglobulin-like receptors and human leukocyte antigen ligands are associated with ankylosing spondylitis.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Revealing the role of natural killer cells in ankylosing spondylitis: identifying diagnostic biomarkers and therapeutic targets.Annals of medicine · 2025Article
- A genetic fingerprint associated with durable HIV remission after interruption of antiretroviral treatment: ANRS VISCONTI/PRIMO.Med (New York, N.Y.) · 2025Article
- Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.Journal of cellular and molecular medicine · 2024Article
- Unveiling the Significance of HLA and KIR Diversity in Underrepresented Populations.Biomedicines · 2024Review
- Biology of HLA class I associated inflammatory diseases.Best practice & research. Clinical rheumatology · 2024Review
- EULAR study group on 'MHC-I-opathy': identifying disease-overarching mechanisms across disciplines and borders.Annals of the rheumatic diseases · 2023Review
- The genetic backbone of ankylosing spondylitis: how knowledge of genetic susceptibility informs our understanding and management of disease.Rheumatology international · 2022Review
- Assessment of HLA-B genetic variation with an HLA-B leader tool and implications in clinical transplantation.Blood advances · 2022Article
- Advances of Genomic Medicine in Psoriatic Arthritis.Journal of personalized medicine · 2022Review
- Contribution of HLA and KIR Alleles to Systemic Sclerosis Susceptibility and Immunological and Clinical Disease Subtypes.Frontiers in genetics · 2022Article
- The role of critical immune genes in brain disorders: insights from neuroimaging immunogenetics.Brain communications · 2022Article
- Mechanistic diversity in MHC class I antigen recognition.The Biochemical journal · 2021Review
- Nanomaterials for the Diagnosis and Treatment of Inflammatory Arthritis.International journal of molecular sciences · 2021Review
- Interaction of HLA Class II rs9272219 andFrontiers in genetics · 2021Article
- HLA-A29 and Birdshot Uveitis: Further Down the Rabbit Hole.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The killer immunoglobulin-like receptors (KIRs), found predominantly on the surface of natural killer (NK) cells and some T-cells, are a collection of highly polymorphic activating and inhibitory receptors with variable specificity for class I human leukocyte antigen (HLA) ligands. Fifteen KIR genes are inherited in haplotypes of diverse gene content across the human population, and the repertoire of independently inherited KIR and HLA alleles is known to alter risk for immune-mediated and infectious disease by shifting the threshold of lymphocyte activation. We have conducted the largest disease-association study of KIR-HLA epistasis to date, enabled by the imputation of KIR gene and HLA allele dosages from genotype data for 12,214 healthy controls and 8,107 individuals with the HLA-B*27-associated immune-mediated arthritis, ankylosing spondylitis (AS). We identified epistatic interactions between KIR genes and their ligands (at both HLA subtype and allele resolution) that increase risk of disease, replicating analyses in a semi-independent cohort of 3,497 cases and 14,844 controls. We further confirmed that the strong AS-association with a pathogenic variant in the endoplasmic reticulum aminopeptidase gene ERAP1, known to alter the HLA-B*27 presented peptidome, is not modified by carriage of the canonical HLA-B receptor KIR3DL1/S1. Overall, our data suggests that AS risk is modified by the complement of KIRs and HLA ligands inherited, beyond the influence of HLA-B*27 alone, which collectively alter the proinflammatory capacity of KIR-expressing lymphocytes to contribute to disease immunopathogenesis.
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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.