ArticleArthritis and rheumatism2012
Expression of HLA-B27 causes loss of migratory dendritic cells in a rat model of spondylarthritis.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Breaking boundaries in ankylosing spondylitis: how innovative cell therapies reshape immunity, drive cutting-edge advances, and face future challenges.Frontiers in immunology · 2025Review
- Microbiome dysbiosis in spinal pathology: Mechanisms, evidence, and research limitations.Brain & spine · 2025Review
- Investigating the causal relationship between immune factors and ankylosing spondylitis: insights from a Mendelian Randomization study.Advances in rheumatology (London, England) · 2024Article
- 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
- Vesicular traffic-mediated cell-to-cell signaling at the immune synapse in Ankylosing Spondylitis.Frontiers in immunology · 2022Review
- Interleukin 27 is a novel cytokine with anti-inflammatory effects against spondyloarthritis through the suppression of Th17 responses.Frontiers in immunology · 2022Article
- Lessons on SpA pathogenesis from animal models.Seminars in immunopathology · 2021Review
- The Role of the IL-23/IL-17 Axis in Disease Initiation in Spondyloarthritis: Lessons Learned From Animal Models.Frontiers in immunology · 2021Review
- Aberrant distribution and function of plasmacytoid dendritic cells in patients with ankylosing spondylitis are associated with unfolded protein response.The Kaohsiung journal of medical sciences · 2020Article
- Dendritic cells in the pathogenesis of ankylosing spondylitis and axial spondyloarthritis.Clinical rheumatology · 2019Review
- Tolerogenic XCR1Arthritis research & therapy · 2019Article
- Effects of the IL-23-IL-17 pathway on bone in spondyloarthritis.Nature reviews. Rheumatology · 2018Review
- The Early Phases of Ankylosing Spondylitis: Emerging Insights From Clinical and Basic Science.Frontiers in immunology · 2018Review
- Role of Stem Cells in Pathophysiology and Therapy of Spondyloarthropathies-New Therapeutic Possibilities?International journal of molecular sciences · 2017Review
- Dysbiosis and zonulin upregulation alter gut epithelial and vascular barriers in patients with ankylosing spondylitis.Annals of the rheumatic diseases · 2017Article
- Perturbed Mucosal Immunity and Dysbiosis Accompany Clinical Disease in a Rat Model of Spondyloarthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- ERAP1 reduces accumulation of aberrant and disulfide-linked forms of HLA-B27 on the cell surface.Molecular immunology · 2016Article
- Non-conventional forms of HLA-B27 are expressed in spondyloarthritis joints and gut tissue.Journal of autoimmunity · 2016Article
- IL-17A deficiency promotes periosteal bone formation in a model of inflammatory arthritis.Arthritis research & therapy · 2016Article
- 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
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveIn rats transgenic for human HLA-B27 and β(2) -microglobulin (B27-transgenic rats), colitis and peripheral inflammation develop spontaneously. Therefore, B27-transgenic rats provide a model of spondylarthritis. Because inflammation in these rats requires CD4+ T lymphocytes and involves intestinal pathology, we hypothesized that dendritic cells (DCs) that migrate from the intestine and control CD4+ T cell differentiation would be aberrant in B27-transgenic rats.
methodsMigrating intestinal lymph DCs were collected via thoracic duct cannulation from B27-transgenic and control (HLA-B7-transgenic or nontransgenic) rats. The phenotypes of these DCs and of mesenteric lymph node DCs were assessed by flow cytometry. The ability of DCs to differentiate from bone marrow precursors in vitro was also assessed.
resultsLymph DCs showed increased activation and, strikingly, lacked the specific DC population that is important for maintaining tolerance to self-antigens. This population of DCs was also depleted from the mesenteric lymph nodes of B27-transgenic rats. Furthermore, in vitro culture of DCs from bone marrow precursors revealed a defect in the ability of B27-transgenic rats to produce DCs of the migratory phenotype, although the DCs that were generated induced enhanced interleukin-17 (IL-17) production from naive CD4+ T cells.
conclusionWe describe 2 different mechanisms by which HLA-B27 may contribute to inflammatory disease: increased apoptotic death of B27-transgenic DCs that normally function to maintain immunologic tolerance and enhanced IL-17 production from CD4+ T cells stimulated by the surviving B27-transgenic DCs.
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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.