ArticleAutoimmunity2013
Endoplasmic reticulum aminopeptidase-1 alleles associated with increased risk of ankylosing spondylitis reduce HLA-B27 mediated presentation of multiple antigens.
Article in Autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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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
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Ankylosing spondylitis risk factors: a systematic literature review.Clinical rheumatology · 2021Pooled it
- Functionally distinct ERAP1 and ERAP2 are a hallmark of HLA-A29-(Birdshot) Uveitis.Human molecular genetics · 2018Pooled it
- Decoding the inflammatory-osteogenic axis in ankylosing spondylitis: mechanisms, dysregulation, and emerging therapeutic interventions.Frontiers in immunology · 2025Review
- FunctionalCells · 2022Article
- A proposed HLA-B*27 screening method for ankylosing spondylitis detection based on tag-single nucleotide polymorphisms: a preliminary study.Molecular biology reports · 2021Article
- Ankylosing spondylitis: an autoimmune or autoinflammatory disease?Nature reviews. Rheumatology · 2021Review
- Understanding the Pathogenesis of Spondyloarthritis.Biomolecules · 2020Review
- Review
- Molecular pathways for antigenic peptide generation by ER aminopeptidase 1.Molecular immunology · 2019Review
- ERAP1 allotypes shape the epitope repertoire of virus-specific CD8Journal of hepatology · 2019Article
- The role of polymorphic ERAP1 in autoinflammatory disease.Bioscience reports · 2018Review
- ERAP1 deficient mice have reduced Type 1 regulatory T cells and develop skeletal and intestinal features of Ankylosing Spondylitis.Scientific reports · 2018Article
- An allelic variant in the intergenic region between ERAP1 and ERAP2 correlates with an inverse expression of the two genes.Scientific reports · 2018Article
- ERAP1/ERAP2 and RUNX3 polymorphisms are not associated with ankylosing spondylitis susceptibility in Chinese Han.Clinical and experimental immunology · 2018Article
- How ERAP1 and ERAP2 Shape the Peptidomes of Disease-Associated MHC-I Proteins.Frontiers in immunology · 2018Review
- The interplay between HLA-B27 and ERAP1/ERAP2 aminopeptidases: from anti-viral protection to spondyloarthritis.Clinical and experimental immunology · 2017Review
- Genome-wide DNA methylation profile analysis identifies differentially methylated loci associated with ankylosis spondylitis.Arthritis research & therapy · 2017Article
- Mice expressing human ERAP1 variants associated with ankylosing spondylitis have altered T-cell repertoires and NK cell functions, as well as increased in utero and perinatal mortality.International immunology · 2017Article
- The Human Leukocyte Antigen (HLA)-B27 PeptidomeMolecular & cellular proteomics : MCP · 2017Article
- Human Leukocyte Antigen (HLA) and Immune Regulation: How Do Classical and Non-Classical HLA Alleles Modulate Immune Response to Human Immunodeficiency Virus and Hepatitis C Virus Infections?Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Ankylosing spondylitis (AS) is a chronic systemic arthritic disease that leads to significant disability and loss of quality of life in the ∼0.5% of the worldwide human population it affects. There is currently no cure for AS and mechanisms underlying its pathogenesis remain unclear. AS is highly genetic, with over 70% of the genetic risk being associated with the presence of HLA-B27 and endoplasmic reticulum aminopeptidase-1 (ERAP1) alleles. Furthermore, gene-gene interactions between HLA-B27 and ERAP1 AS risk alleles have recently been confirmed. Here, we demonstrate that various ERAP1 alleles can differentially mediate surface expression of antigens presented by HLA-B27 on human cells. Specifically, for all peptides tested, we found that an ERAP1 variant containing high AS risk SNPs reduced the amount of the peptide presented by HLA-B27, relative to low AS risk ERAP1 variants. These results were further validated using peptide catalysis assays in vitro, suggesting that high AS risk alleles have an enhanced catalytic activity that more rapidly destroys many HLA-B27-destined peptides, a result that correlated with decreased HLA-B27 presentation of the same peptides. These findings suggest that one mechanism underlying AS pathogenesis may involve an altered ability for AS patients harboring both HLA-B27 and high AS risk ERAP1 alleles to correctly display a variety of peptides to the adaptive arm of the immune system, potentially exposing such individuals to higher AS risk due to abnormal display of pathogen or self-derived peptides by the adaptive immune system.
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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.