ArticleMolecular immunology2016
ERAP1 reduces accumulation of aberrant and disulfide-linked forms of HLA-B27 on the cell surface.
Article in Molecular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- HLA-B27 and spondyloarthritis: at the crossroads of innate and adaptive immunity.Nature reviews. Rheumatology · 2025Review
- Sequence of Events in the Pathogenesis of Axial Spondyloarthritis: A Current Review-2023 SPARTAN Meeting Proceedings.Current rheumatology reports · 2024Review
- Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023Review
- Paradoxical Effects of Endoplasmic Reticulum Aminopeptidase 1 Deficiency on HLA-B27 and Its Role as an Epistatic Modifier in Experimental Spondyloarthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Spondyloarthritides: Theories and beyond.Frontiers in pediatrics · 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
- Redundancy and Complementarity between ERAP1 and ERAP2 Revealed by their Effects on the Behcet's Disease-associated HLA-B*51 Peptidome.Molecular & cellular proteomics : MCP · 2019Article
- HLA associations in inflammatory arthritis: emerging mechanisms and clinical implications.Nature reviews. Rheumatology · 2019Review
- Unmet Needs in Axial Spondyloarthritis.Clinical reviews in allergy & immunology · 2018Review
- Association of ERAP1 gene polymorphisms with the susceptibility to psoriasis vulgaris: A case-control study.Medicine · 2018Observational
- An allelic variant in the intergenic region between ERAP1 and ERAP2 correlates with an inverse expression of the two genes.Scientific reports · 2018Article
- Polymorphisms of human leukocyte antigen B*27 on clinical phenotype of spondyloarthritis in Chinese.Journal of clinical laboratory analysis · 2018Article
- Distinct mechanisms survey the structural integrity of HLA-B*27:05 intracellularly and at the surface.PloS one · 2018Article
- 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
- Recent advances in understanding spondyloarthritis.F1000Research · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveEndoplasmic reticulum (ER) aminopeptidase 1 (ERAP1) variants contribute to the risk of ankylosing spondylitis in HLA-B27 positive individuals, implying a disease-related interaction between these gene products. The aim of this study was to determine whether reduced ERAP1 expression would alter the cell surface expression of HLA-B27 and the formation of aberrant disulfide-linked forms that have been implicated in the pathogenesis of spondyloarthritis.
methodsERAP1 expression was knocked down in monocytic U937 cells expressing HLA-B27 and endogenous HLA class I. The effect of ERAP1 knockdown on the accumulation HLA-B alleles (B18, B51, and B27) was assessed using immunoprecipitation, isoelectric focusing, and immunoblotting, as well as flow cytometry with antibodies specific for different forms of HLA-B27. Cell surface expression of aberrant disulfide-linked HLA-B27 dimers was assessed by immunoprecipitation and electrophoresis on non-reducing polyacrylamide gels.
resultsERAP1 knockdown increased the accumulation of HLA-B27 on the cell surface including disulfide-linked dimers, but had no effect on levels of HLA-B18 or -B51. Antibodies with unique specificity for HLA-B27 confirmed increased cell surface expression of complexes shown previously to contain long peptides. IFN-γ treatment resulted in striking increases in the expression of disulfide-linked HLA-B27 heavy chains, even in cells with normal ERAP1 expression.
conclusionsOur results suggest that normal levels of ERAP1 reduce the accumulation of aberrant and disulfide-linked forms of HLA-B27 in monocytes, and thus help to maintain the integrity of cell surface HLA-B27 complexes.
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