ArticleGenes and immunity
Disease-associated polymorphisms in ERAP1 do not alter endoplasmic reticulum stress in patients with ankylosing spondylitis.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Unveiling the impact of ERAP1 and ERAP2 on migration, angiogenesis and ER stress response.Frontiers in cell and developmental biology · 2025Review
- 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
- HLA-B27 may modulate the interaction between ERAP1 polymorphisms and smoking in ankylosing spondylitis patients.Molecular biology reports · 2022Article
- HLA associations in inflammatory arthritis: emerging mechanisms and clinical implications.Nature reviews. Rheumatology · 2019Review
- Stress proteins in the pathogenesis of spondyloarthritis.Rheumatology international · 2019Review
- Ankylosing spondylitis: etiology, pathogenesis, and treatments.Bone research · 2019Article
- The interplay between HLA-B27 and ERAP1/ERAP2 aminopeptidases: from anti-viral protection to spondyloarthritis.Clinical and experimental immunology · 2017Review
- Genetics and the Causes of Ankylosing Spondylitis.Rheumatic diseases clinics of North America · 2017Review
- Pathogenesis of ankylosing spondylitis - recent advances and future directions.Nature reviews. Rheumatology · 2017Review
- ERAP1 rs30187 single nucleotide polymorphism does not confer disease susceptibility in North Indian children with enthesitis-related arthritis.Clinical rheumatology · 2017Article
- Role of HLA-B27 in the pathogenesis of ankylosing spondylitis (Review).Molecular medicine reports · 2017Review
- Silencing or inhibition of endoplasmic reticulum aminopeptidase 1 (ERAP1) suppresses free heavy chain expression and Th17 responses in ankylosing spondylitis.Annals of the rheumatic diseases · 2016Article
- Genetics of ankylosing spondylitis--insights into pathogenesis.Nature reviews. Rheumatology · 2016Review
- Ankylosing spondylitis patients display altered dendritic cell and T cell populations that implicate pathogenic roles for the IL-23 cytokine axis and intestinal inflammation.Rheumatology (Oxford, England) · 2016Article
- Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1.Nature communications · 2015Article
- The genetic associations of acute anterior uveitis and their overlap with the genetics of ankylosing spondylitis.Genes and immunityArticle
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism by which human leukocyte antigen B27 (HLA-B27) contributes to ankylosing spondylitis (AS) remains unclear. Genetic studies demonstrate that association with and interaction between polymorphisms of endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 influence the risk of AS. It has been hypothesised that ERAP1-mediated HLA-B27 misfolding increases endoplasmic reticulum (ER) stress, driving an interleukin (IL) 23-dependent, pro-inflammatory immune response. We tested the hypothesis that AS-risk ERAP1 variants increase ER-stress and concomitant pro-inflammatory cytokine production in HLA-B27(+) but not HLA-B27(-) AS patients or controls. Forty-nine AS cases and 22 healthy controls were grouped according to HLA-B27 status and AS-associated ERAP1 rs30187 genotypes: HLA-B27(+)ERAP1(risk), HLA-B27(+)ERAP1(protective), HLA-B27(-)ERAP1(risk) and HLA-B27(-)ERAP1(protective). Expression levels of ER-stress markers GRP78 (8 kDa glucose-regulated protein), CHOP (C/EBP-homologous protein) and inflammatory cytokines were determined in peripheral blood mononuclear cell and ileal biopsies. We found no differences in ER-stress gene expression between HLA-B27(+) and HLA-B27(-) cases or healthy controls, or between cases or controls stratified by carriage of ERAP1 risk or protective alleles in the presence or absence of HLA-B27. No differences were observed between expression of IL17A or TNF (tumour necrosis factor) in HLA-B27(+)ERAP1(risk), HLA-B27(+)ERAP1(protective) and HLA-B27(-)ERAP1(protective) cases. These data demonstrate that aberrant ERAP1 activity and HLA-B27 carriage does not alter ER-stress levels in AS, suggesting that ERAP1 and HLA-B27 may influence disease susceptibility through other mechanisms.
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