ArticleThe Journal of experimental medicine1985
Immune complexes can trigger specific, T cell-dependent, autoanti-IgG antibody production in mice.
Article in The Journal of experimental medicine, 1985. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The trial behind it
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Who cites it
35 citing papers in PubMed, 125 citations in OpenAlex.
- Comparative analysis of immunological responses to oral (Ty21a) and parenteral (TAB) typhoid vaccines.Infection and immunity · 1988Trial
- Article
- The role of large immune complexes in anti-drug antibody development: a case study of anti-SARS-CoV-2 antibody therapeutics and co-administered mRNA vaccine.Frontiers in immunology · 2026Article
- Immunogenicity Risk Assessment for Multi-specific Therapeutics.The AAPS journal · 2021Review
- The immunopathogenesis of seropositive rheumatoid arthritis: from triggering to targeting.Nature reviews. Immunology · 2017Review
- Neutralization-Enhancing RF Antibodies for HIV Vaccines.Frontiers in immunology · 2014Review
- Rapid vaccination using an acetalated dextran microparticulate subunit vaccine confers protection against triplicate challenge by bacillus anthracis.Pharmaceutical research · 2013Article
- Anti-chromatin antibodies drive in vivo antigen-specific activation and somatic hypermutation of rheumatoid factor B cells at extrafollicular sites.European journal of immunology · 2007Article
- Regulation of lupus-related autoantibody production and clinical disease by Toll-like receptors.Seminars in immunology · 2007Review
- Role of repetitive antigen patterns for induction of antibodies against antibodies.The Journal of experimental medicine · 1997Article
- When do microbes stimulate rheumatoid factor?The Journal of experimental medicine · 1997Review
- Peripheral deletion of rheumatoid factor B cells after abortive activation by IgG.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Activation of effector functions by immune complexes of mouse IgG2a with isotype-specific autoantibodies.Immunology · 1995Article
- Human immunoglobulin (IgG) induced deletion of IgM rheumatoid factor B cells in transgenic mice.The Journal of experimental medicine · 1995Article
- Control of autoantibody affinity by selection against amino acid replacements in the complementarity-determining regions.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Adjuvant arthritis is associated with changes in the glycosylation of serum IgG1 and IgG2b.Clinical and experimental immunology · 1993Article
- Rheumatoid factor production by mononuclear cells derived from different sites of patients with rheumatoid arthritis.Clinical and experimental immunology · 1993Article
- Spontaneous in vitro production of rheumatoid factor during infectious exacerbations of cystic fibrosis: correlation with circulating immune complex levels.Clinical and experimental immunology · 1993Article
- Production of rheumatoid factor in adoptively immune guinea-pigs after challenge with Treponema pallidum.Immunology · 1992Article
- Feedback regulation of antibody production: a role in rheumatoid arthritis?Annals of the rheumatic diseases · 1991Review
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunization of mice with a combination of passively administered syngeneic IgG (anti-p-azophenylarsonate [anti-Ars]) antibody and a soluble, multivalent form of the antibody's corresponding antigen (Limulus polyphemus hemocyanin conjugated with Ars [Lph-Ars]) resulted in specific autoanti-IgG Fc (rheumatoid factor) production. The response was rapid and only anti-IgG of the IgM isotype is found. Because immunization with either the IgG antibody or the antigen alone did not result in rheumatoid antibody production, immune complexes appear to be the active form of the immunogens. Antibody/antigen ratios that resulted in maximal anti-IgG antibody responses were the same as those required for peak in vitro immunoprecipitation, i.e., equivalence. Previous exposure of the mice to the exogenously supplied antigen was not required for the response. The response to immune complexes is specific because mice immunized with IgG2a-containing complexes produced autoanti-IgG2a, while mice immunized with IgG1-containing complexes produced anti-IgG1 with little reactivity to other IgG isotypes. IgG2a blocked in its complement-fixing capacity was more effective in eliciting the anti-IgG2a response than native IgG2a, suggesting a possible role for the complement system in modulating the anti-IgG2a response. Induction of rheumatoid factor production by immune complexes could be induced in xid mice but not in nu/nu mice, indicating T lymphocyte dependence of the response. In contrast, the B lymphocyte activator lipopolysaccharide was able to elicit vigorous rheumatoid factor production in both nu/nu and normal mice, demonstrating that nu/nu mice contain B cells capable of making the response. Rheumatoid antibody produced in the immune complex- or LPS-induced responses is Fc specific and has relatively low affinity for IgG that is not bound to antigen.
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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.