ArticleThe Journal of clinical investigation1990
Regulation of the anti-Sm autoantibody response in systemic lupus erythematosus mice by monoclonal anti-Sm antibodies.
Article in The Journal of clinical investigation, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement.The Journal of experimental medicine · 2005Article
- Mechanisms of autoimmunity.Immunologic research · 2003Review
- Regulation of autoreactive anti-IgG (rheumatoid factor) B cells in normal and autoimmune mice.Immunologic research · 1999Review
- Further characterization of the autoantibody response of Palmerston North mice.Journal of clinical immunology · 1999Article
- Features of autoantigens.Molecular biology reports · 1996Review
- Pathogenic natural anti-cardiolipin antibodies: the experience from monoclonal gammopathy.Clinical and experimental immunology · 1994Article
- Pathogenic serum IgG anticardiolipin antibodies and the idiotypic network.Annals of the rheumatic diseases · 1993Article
- Anti-Sm autoantibodies in systemic lupus erythematosus mice: a model system for disease-specific autoreactivity.Springer seminars in immunopathology · 1992Review
- Lessons about autoantibody specificity in systemic lupus erythematosus from animal models.Clinical and experimental immunology · 1990Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The administration of certain monoclonal anti-Sm antibodies (2G7, 7.13) induced most MRL/lpr mice to become anti-Sm positive by 5 mo of age, although other anti-Sm monoclonals (Y2, Y12) suppressed the spontaneous response. Positive anti-Sm antibody enhancement occurred efficiently only in MRL/lpr mice and not in other systemic lupus erythematosus mice that have little spontaneous anti-Sm production. The enhancement by anti-Sm antibodies was specific for the anti-Sm response. The mechanism of the passive antibody enhancement was apparently not isotype- or idiotype-related. The fine specificity of the anti-Sm monoclonal antibody may be essential to its enhancing or suppressing effects, since both enhancing monoclonals recognized only the D Sm polypeptide, whereas both suppressing monoclonals saw the D and the B polypeptides. Furthermore, analysis of serial bleeds from unmanipulated MRL mice that developed anti-Sm positivity showed that the D specificity almost always appeared first. We hypothesize, therefore, that those animals in which an anti-Sm response is initiated by D-specific B-cell clones can become serologically positive with the aid of a positive feedback loop. In contrast, animals in which the initial specificity is for both B and D peptides would be prevented from developing a full anti-Sm response.
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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.