ArticleMolecular immunology2007
B cells are important as antigen presenting cells for induction of MHC-restricted arthritis in transgenic mice.
Article in Molecular immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 30 citations in OpenAlex.
- B cells drive CD4 T cell immunosenescence and age-associated health decline.Science immunology · 2026Article
- Fc-enhanced anti-CCR6 antibody elicits robust therapeutic effects across multiple autoimmune diseases.Frontiers in immunology · 2025Article
- Review
- Overview of Rheumatoid Arthritis and Scientific Understanding of the Disease.Mediterranean journal of rheumatology · 2023Review
- Modulation of co-stimulatory signal from CD2-CD58 proteins by a grafted peptide.Chemical biology & drug design · 2021Article
- Constrained Cyclic Peptides as Immunomodulatory Inhibitors of the CD2:CD58 Protein-Protein Interaction.ACS chemical biology · 2016Article
- Article
- Cytokines pre-determined by genetic factors are involved in pathogenesis of Rheumatoid arthritis.Cytokine · 2015Article
- Arthritis susceptibility and the gut microbiome.FEBS letters · 2014Review
- DRB1*0402 may influence arthritis by promoting naive CD4+ T-cell differentiation in to regulatory T cells.European journal of immunology · 2014Article
- Anti-citrullinated protein antibodies: role in pathogenesis of RA and potential as a diagnostic tool.Rheumatology international · 2013Review
- To B or not to B: role of B cells in pathogenesis of arthritis in HLA transgenic mice.Journal of autoimmunity · 2011Review
- Conformationally constrained peptides from CD2 to modulate protein-protein interactions between CD2 and CD58.Journal of medicinal chemistry · 2011Article
- Mechanism by which HLA-DR4 regulates sex-bias of arthritis in humanized mice.Journal of autoimmunity · 2010Article
- Role of B cells in systemic lupus erythematosus and rheumatoid arthritis.Current opinion in immunology · 2008Article
- Cellular and humoral immunity in arthritis are profoundly influenced by the interaction between cigarette smoke effects and host HLA-DR and DQ genes.Clinical immunology (Orlando, Fla.)Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Rheumatoid arthritis and its animal model, collagen-induced arthritis, are known as a T and B cell dependent disease. To analyze the role of B cells in arthritis, we generated B cell deficient (microMT) mice carrying HLA-DQ8 as transgene, Abetao.DQ8.micromt mice. HLA-DQ8 transgenic mice (Abetao.DQ8) are susceptible to collagen induced arthritis, an animal model for inflammatory arthritis. Deletion of IgM gene led to the absence of B cells while T cells were comparable to Abetao.DQ8 mice. Arthritis and autoantibodies was completely abrogated in B cell deficient DQ8 mice. T cell response and proinflammatory cytokine production in response to type II collagen and its derived peptides in vitro was significantly decreased despite an increased number of Mac-1 positive cells in DQ8.micromt mice compared to DQ8 mice suggesting B cells could be important for antigen presentation as well. In vitro substitution of B cells from wild type mice restored the response in DQ8.micromt mice. B cells could also present CII-derived peptides to antigen-specific DQ8-restricted hybridomas reinforcing the role of B cells in presentation of antigens to T cells. The data suggest that B cells can be involved in pathogenesis of arthritis by producing autoantibodies and antigen presentation.
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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.