ArticleJournal of immunology (Baltimore, Md. : 1950)2013
A small shared epitope-mimetic compound potently accelerates osteoclast-mediated bone damage in autoimmune arthritis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Anti-Inflammatory Effects of Clarstatin, a Shared-Epitope-Antagonistic Cyclic Peptide, on Experimental Autoimmune Uveitis in Mice.Investigative ophthalmology & visual science · 2025Article
- Development of Clarstatin, a Novel Drug Lead for the Therapy of Autoimmune Uveitis.Pharmaceutics · 2024Article
- Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- HLA-G and the MHC Cusp Theory.Frontiers in immunology · 2022Review
- HLA-DRB1 allelic epitopes that associate with autoimmune disease risk or protection activate reciprocal macrophage polarization.Scientific reports · 2021Article
- Uncovering a Shared Epitope-Activated Protein Citrullination Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- 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
- 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
- Spontaneous destructive periodontitis and skeletal bone damage in transgenic mice carrying a human shared epitope-codingRMD open · 2016Article
- Shared epitope-antagonistic ligands: a new therapeutic strategy in mice with erosive arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- The quest for better understanding of HLA-disease association: scenes from a road less travelled by.Discovery medicine · 2013Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
We have recently proposed that the shared epitope (SE) may contribute to rheumatoid arthritis pathogenesis by acting as a ligand that activates proarthritogenic signal transduction events. To examine this hypothesis, in this study we characterized a novel small SE-mimetic compound, c(HS4-4), containing the SE primary sequence motif QKRAA, which was synthesized using a backbone cyclization method. The SE-mimetic c(HS4-4) compound interacted strongly with the SE receptor calreticulin, potently activated NO and reactive oxygen species production, and markedly facilitated osteoclast differentiation and function in vitro. The pro-osteoclastogenic potency of c(HS4-4) was 100,000- to 1,000,000-fold higher than the potency of a recently described linear SE peptidic ligand. When administered in vivo at nanogram doses, c(HS4-4) enhanced Th17 expansion, and in mice with collagen-induced arthritis it facilitated disease onset, increased disease incidence and severity, enhanced osteoclast abundance in synovial tissues and osteoclastogenic propensities of bone marrow-derived cells, and augmented bone destruction. In conclusion, c(HS4-4), a highly potent small SE-mimetic compound enhances bone damage and disease severity in inflammatory arthritis. These findings support the hypothesis that the SE acts as a signal transduction ligand that activates a CRT-mediated proarthritogenic pathway.
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Registered trials
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.