ArticleProceedings of the National Academy of Sciences of the United States of America2008
Editing and escape from editing in anti-DNA B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- IQGAP1 promotes early B cell development, is essential for the development of marginal zone (MZ) B cells, and is critical for both T-dependent and T-independent antibody responses.Cellular and molecular life sciences : CMLS · 2024Article
- SLE: a cognitive step forward-a synthesis of rethinking theories, causality, and ignored DNA structures.Frontiers in immunology · 2024Review
- The greatest contribution to medical science is the transformation from studying symptoms to studying their causes-the unrelenting legacy of Robert Koch and Louis Pasteur-and a causality perspective to approach a definition of SLE.Frontiers in immunology · 2024Article
- The Anti-DNA Antibodies: Their Specificities for Unique DNA Structures and Their Unresolved Clinical Impact-A System Criticism and a Hypothesis.Frontiers in immunology · 2021Review
- Autoimmunity and SLE: Factual and Semantic Evidence-Based Critical Analyses of Definitions, Etiology, and Pathogenesis.Frontiers in immunology · 2020Review
- Systemic Lupus Erythematosus: Definitions, Contexts, Conflicts, Enigmas.Frontiers in immunology · 2018Article
- VprBP Is Required for Efficient Editing and Selection of Igκ+ B Cells, but Is Dispensable for Igλ+ and Marginal Zone B Cell Maturation and Selection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Predominant role for activation-induced cytidine deaminase in generating IgG anti-nucleosomal antibodies of murine SLE.Journal of autoimmunity · 2015Article
- SLAP deficiency decreases dsDNA autoantibody production.Clinical immunology (Orlando, Fla.) · 2014Article
- Trials and Tribulations with VH Replacement.Frontiers in immunology · 2014Review
- Antibodies that bind complex glycosaminoglycans accumulate in the Golgi.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- B-cell tolerance defects in the B6.Aec1/2 mouse model of Sjögren's syndrome.Journal of clinical immunology · 2012Article
- Apoptotic marginal zone deletion of anti-Sm/ribonucleoprotein B cells.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Accumulation of B1-like B cells in transgenic mice over-expressing catalytically inactive RAG1 in the periphery.Immunology · 2011Article
- B cell receptor editing in tolerance and autoimmunity.Annals of the New York Academy of Sciences · 2011Review
- A new site-directed transgenic rheumatoid factor mouse model demonstrates extrafollicular class switch and plasmablast formation.Autoimmunity · 2010Article
- Regulation of the B cell receptor repertoire and self-reactivity by BAFF.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Checkpoints in lymphocyte development and autoimmune disease.Nature immunology · 2010Review
- Antibodies in a heavy chain knock-in mouse exhibit characteristics of early heavy chain rearrangement.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tolerance to dsDNA is achieved through editing of Ig receptors that react with dsDNA. Nevertheless, some B cells with anti-dsDNA receptors escape editing and migrate to the spleen. Certain anti-dsDNA B cells that are recovered as hybridomas from the spleens of anti-dsDNA H chain transgenic mice also bind an additional, Golgi-associated antigen. B cells that bind this antigen accumulate intracellular IgM. The intracellular accumulation of IgM is incomplete, because IgM clusters are observed at the cell surface. In the spleen, B cells that express the heavy and light chains encoding this IgM are surface IgM-bright and acquire the CD21-high/CD23-low phenotype of marginal zone B cells. Our data imply that expression of an Ig that binds dsDNA and an additional antigen expressed in the secretory compartment renders B cells resistant to central tolerance. In the periphery, these B cells may be sequestered in the splenic marginal zone.
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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.