ArticleArthritis and rheumatism2009
HLA-B27 misfolding and the unfolded protein response augment interleukin-23 production and are associated with Th17 activation in transgenic rats.
Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers.
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Who cites it
192 citing papers in PubMed, 388 citations in OpenAlex.
- Activating killer immunoglobulin-like receptors genes are associated with increased susceptibility to ankylosing spondylitis.Clinical and experimental immunology · 2015Trial
- Zhuangdu Quhan Mixture Alleviates Ankylosing Spondylitis in Mice by Inhibiting the Interleukin-17 Signaling.Biomedical chromatography : BMC · 2026Article
- Immunometabolic regulation and tissue-resident immunity in autoimmune uveitis: from genetic susceptibility to the gut-spleen-eye axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Recent Advances in the Pharmacological Management of Pediatric Spondyloarthritis.Paediatric drugs · 2026Review
- Association between systemic inflammation-immune index and comorbidities in patients with ankylosing spondylitis: a cross-sectional study.Clinical rheumatology · 2026Article
- Mechanistic Insights from Human Studies in Axial Spondyloarthritis: A T Cell Story.Current rheumatology reports · 2026Review
- Genetically predicted susceptibility to dust-induced lung diseases and risk of autoimmune diseases: a two sample Mendelian randomization study.Journal of neuroinflammation · 2026Article
- Rapamycin treatment ameliorates HLA-B27-mediated gut inflammation and alters the microbiome in experimental spondyloarthritis.Frontiers in immunology · 2026Article
- What can Animal Models tell us About T Cells in Spondyloarthritis Pathogenesis?Current rheumatology reports · 2025Review
- Granulocyte-macrophage colony-stimulating factor may contribute to spondyloarthritis development in HLA-B27 transgenic rat by affecting conventional dendritic cells function.Arthritis research & therapy · 2025Article
- [Microbial and genetic factors in the pathogenesis of spondyloarthritis].Zeitschrift fur Rheumatologie · 2025Article
- Pathogenesis of psoriatic arthritis: new insights from a bone marrow perspective.Current opinion in rheumatology · 2025Review
- HLA-B27 and spondyloarthritis: at the crossroads of innate and adaptive immunity.Nature reviews. Rheumatology · 2025Review
- Emerging biochemical, microbial and immunological evidence in the search for why HLA-BCell chemical biology · 2025Review
- Unveiling the impact of ERAP1 and ERAP2 on migration, angiogenesis and ER stress response.Frontiers in cell and developmental biology · 2025Review
- Breaking boundaries in ankylosing spondylitis: how innovative cell therapies reshape immunity, drive cutting-edge advances, and face future challenges.Frontiers in immunology · 2025Review
- A brief overview of SARS-CoV-2 infection and its management strategies: a recent update.Molecular and cellular biochemistry · 2024Review
- Complex Interactions between the Human Major Histocompatibility Complex (MHC) and Microbiota: Their Roles in Disease Pathogenesis and Immune System Regulation.Biomedicines · 2024Review
- Dysregulated Non-Coding RNA Expression in T Cells from Patients with Ankylosing Spondylitis Contributes to Its Immunopathogenesis.Biomedicines · 2024Review
132 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo determine whether HLA-B27 misfolding and the unfolded protein response (UPR) result in cytokine dysregulation and whether this is associated with Th1 and/or Th17 activation in HLA-B27/human beta(2)-microglobulin (Hubeta(2)m)-transgenic rats, an animal model of spondylarthritis.
methodsCytokine expression in lipopolysaccharide (LPS)-stimulated macrophages was analyzed in the presence and absence of a UPR induced by chemical agents or by HLA-B27 up-regulation. Cytokine expression in colon tissue and in cells purified from the lamina propria was determined by real-time reverse transcription-polymerase chain reaction analysis, and differences in Th1 and Th17 CD4+ T cell populations were quantified after intracellular cytokine staining.
resultsInterleukin-23 (IL-23) was found to be synergistically up-regulated by LPS in macrophages undergoing a UPR induced by pharmacologic agents or by HLA-B27 misfolding. IL-23 was also increased in the colon tissue from B27/Hubeta(2)m-transgenic rats concurrently with the development of intestinal inflammation, and IL-17, a downstream target of IL-23, exhibited robust up-regulation in a similar temporal pattern. IL-23 and IL-17 transcripts were localized to CD11+ antigen-presenting cells and CD4+ T cells, respectively, from the colonic lamina propria. Colitis was associated with a 6-fold expansion of CD4+ IL-17-expressing T cells.
conclusionThe IL-23/IL-17 axis is strongly activated in the colon of B27/Hubeta(2)m-transgenic rats with spondylarthritis-like disease. HLA-B27 misfolding and UPR activation in macrophages can result in enhanced induction of the pro-Th17 cytokine IL-23. These results suggest a possible link between HLA-B27 misfolding and immune dysregulation in this animal model, with implications for human disease.
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