ReviewSeminars in immunopathology2021
Aberrant antigen processing and presentation: Key pathogenic factors leading to immune activation in Ankylosing spondylitis.
Review in Seminars in immunopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Single-immunocyte transcriptomics reveal the role of natural killer cell-dependent exogenous antigen presentation in ankylosing spondylitis severity.Experimental & molecular medicine · 2026Article
- Inflammatory cytokines mediate the common genetic and immunological background between rheumatoid arthritis and osteoporosis.Clinical rheumatology · 2026Article
- Single-cell immunomics reveals the immunological hallmarks about the onset and different outcomes for ankylosing spondylitis patients.Clinical rheumatology · 2025Article
- Recent Advances in the Immunopathology of Axial Spondyloarthritis: with and without HLA-B27.Current rheumatology reports · 2025Review
- JAK inhibition and axial spondyloarthritis: new steps on the path to understanding pathophysiology.Frontiers in immunology · 2025Review
- Year in Review: Novel Insights in the Pathogenesis of Spondyloarthritis - SPARTAN 2024 Annual Meeting Proceedings.Current rheumatology reports · 2024Review
- Sequence of Events in the Pathogenesis of Axial Spondyloarthritis: A Current Review-2023 SPARTAN Meeting Proceedings.Current rheumatology reports · 2024Review
- Impact of endoplasmic reticulum aminopeptidases 1 (ERAP1) and 2 (ERAP2) on neutrophil cellular functions.Frontiers in cell and developmental biology · 2024Article
- Regulation mechanisms of disulfidptosis-related genes in ankylosing spondylitis and inflammatory bowel disease.Frontiers in immunology · 2024Article
- Updates on ankylosing spondylitis: pathogenesis and therapeutic agents.Journal of rheumatic diseases · 2023Review
- Human Leukocyte Antigen B27-Negative Axial Spondyloarthritis: What Do We Know?ACR open rheumatology · 2023Review
- Exploring hub pyroptosis-related genes, molecular subtypes, and potential drugs in ankylosing spondylitis by comprehensive bioinformatics analysis and molecular docking.BMC musculoskeletal disorders · 2023Article
- Novel Autophagy-Related Blood Biomarkers Associated with Immune Cell Infiltration in Ankylosing Spondylitis.Pharmacogenomics and personalized medicine · 2023Article
- The genetic backbone of ankylosing spondylitis: how knowledge of genetic susceptibility informs our understanding and management of disease.Rheumatology international · 2022Review
- Construction of an immune-related ceRNA network to screen for potential diagnostic markers for autism spectrum disorder.Frontiers in genetics · 2022Article
- Vesicular traffic-mediated cell-to-cell signaling at the immune synapse in Ankylosing Spondylitis.Frontiers in immunology · 2022Review
- Recent advances in spondyloarthritis: positive developments in the seronegative domain.Seminars in immunopathology · 2021Article
- The Potential Role of Genetics, Environmental Factors, and Gut Dysbiosis in the Aberrant Non-Coding RNA Expression to Mediate Inflammation and Osteoclastogenic/Osteogenic Differentiation in Ankylosing Spondylitis.Frontiers in cell and developmental biology · 2021Review
- Integrative Single-Cell RNA-Seq and ATAC-Seq Analysis of Peripheral Mononuclear Cells in Patients With Ankylosing Spondylitis.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The strong association of HLA-B*27 with ankylosing spondylitis (AS) was first reported nearly 50 years ago. However, the mechanistic link between HLA-B*27 and AS has remained an enigma. While 85-90% of AS patients possess HLA-B*27, majority of HLA-B*27 healthy individuals do not develop AS. This suggests that additional genes and genetic regions interplay with HLA-B*27 to cause AS. Previous genome-wide association studies (GWAS) identified key genes that are distinctively expressed in AS, including the Endoplasmic Reticulum Aminopeptidase (ERAP) 1 and ERAP2. As these gene-encoding molecules are primarily implicated in the process of peptide processing and presentation, potential pathological interaction of these molecules with HLA-B*27 may operate to cause AS by activating downstream immune responses. The aberrant peptide processing also gives rise to the accumulation of unstable protein complex in endoplasmic reticulum (ER), which drives endoplasmic reticulum-associated protein degradation (ERAD) and unfolded protein response (UPR) and activates autophagy. In this review, we describe the current hypotheses of AS pathogenesis, focusing on antigen processing and presentation operated by HLA-B*27 and associated molecules that may contribute to the disease initiation and progression of AS.
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