ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Immune dysregulation by the rheumatoid arthritis shared epitope.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- Genetic susceptibility of human leukocyte antigen alleles in chronic inflammatory demyelinating polyneuropathy in Korean patients : Short title: HLA alleles and CIDP in Korea.BMC neurology · 2025Article
- The Role of Alarmins in the Pathogenesis of Rheumatoid Arthritis, Osteoarthritis, and Psoriasis.Current issues in molecular biology · 2024Review
- Rheumatoid arthritis and the intestinal microbiome: probiotics as a potential therapy.Frontiers in immunology · 2024Review
- Indigenous Nigeria medicinal herbal remedies: A potential source for therapeutic against rheumatoid arthritis.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- HLA-G and the MHC Cusp Theory.Frontiers in immunology · 2022Review
- Uncovering a Shared Epitope-Activated Protein Citrullination Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Interleukin-17 in rheumatoid arthritis: Trials and tribulations.The Journal of experimental medicine · 2020Review
- Linkage of Periodontitis and Rheumatoid Arthritis: Current Evidence and Potential Biological Interactions.International journal of molecular sciences · 2019Review
- HLA associations in inflammatory arthritis: emerging mechanisms and clinical implications.Nature reviews. Rheumatology · 2019Review
- Shared epitope-aryl hydrocarbon receptor crosstalk underlies the mechanism of gene-environment interaction in autoimmune arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Human Leukocyte Antigen-Disease Associations in Rheumatoid Arthritis.Rheumatic diseases clinics of North America · 2017Review
- HLA-DRB1 the notorious gene in the mosaic of autoimmunity.Immunologic research · 2017Article
- A reciprocal HLA-Disease Association in Rheumatoid Arthritis and Pemphigus Vulgaris.Frontiers in bioscience (Landmark edition) · 2017Review
- Periodontal bacterial colonization in synovial tissues exacerbates collagen-induced arthritis in B10.RIII mice.Arthritis research & therapy · 2016Article
- Common Genetic Variants Found in HLA and KIR Immune Genes in Autism Spectrum Disorder.Frontiers in neuroscience · 2016Review
- Spontaneous destructive periodontitis and skeletal bone damage in transgenic mice carrying a human shared epitope-codingRMD open · 2016Article
- Cytokines pre-determined by genetic factors are involved in pathogenesis of Rheumatoid arthritis.Cytokine · 2015Article
- Shared epitope-antagonistic ligands: a new therapeutic strategy in mice with erosive arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Interaction between extracellular matrix molecules and microbial pathogens: evidence for the missing link in autoimmunity with rheumatoid arthritis as a disease model.Frontiers in microbiology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Rheumatoid arthritis (RA) is closely associated with HLA-DRB1 alleles that code a five-amino acid sequence motif in positions 70-74 of the HLA-DRbeta-chain, called the shared epitope (SE). The mechanistic basis of SE-RA association is unknown. We recently found that the SE functions as an allele-specific signal-transducing ligand that activates an NO-mediated pathway in other cells. To better understand the role of the SE in the immune system, we examined its effect on T cell polarization in mice. In CD11c(+)CD8(+) dendritic cells (DCs), the SE inhibited the enzymatic activity of indoleamine 2,3 dioxygenase, a key enzyme in immune tolerance and T cell regulation, whereas in CD11c(+)CD8(-) DCs, the ligand activated robust production of IL-6. When SE-activated DCs were cocultured with CD4(+) T cells, the differentiation of Foxp3(+) T regulatory cells was suppressed, whereas Th17 cells were expanded. The polarizing effects could be seen with SE(+) synthetic peptides, but even more so when the SE was in its natural tridimensional conformation as part of HLA-DR tetrameric proteins. In vivo administration of the SE ligand resulted in a greater abundance of Th17 cells in the draining lymph nodes and increased IL-17 production by splenocytes. Thus, we conclude that the SE acts as a potent immune-stimulatory ligand that can polarize T cell differentiation toward Th17 cells, a T cell subset that was recently implicated in the pathogenesis of autoimmune diseases, including RA.
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