ArticleMolecular immunology2009
Molecular hallmarks of anti-chromatin antibodies associated with the lupus susceptibility locus, Sle1.
Article in Molecular immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 10 citations in OpenAlex.
- FasClinical immunology (Orlando, Fla.) · 2024Article
- Two Distinct Pathways in Mice Generate Antinuclear Antigen-Reactive B Cell Repertoires.Frontiers in immunology · 2018Article
- Antibody Epitope Specificity for dsDNA Phosphate Backbone Is an Intrinsic Property of the Heavy Chain Variable Germline Gene Segment Used.Frontiers in immunology · 2018Article
- Role of Sex Hormone Levels and Psychological Stress in the Pathogenesis of Autoimmune Diseases.Cureus · 2017Review
- Loss of Immune Tolerance Is Controlled by ICOS in Sle1 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Dual-reactive B cells are autoreactive and highly enriched in the plasmablast and memory B cell subsets of autoimmune mice.The Journal of experimental medicine · 2012Article
- Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Anti-nuclear antibody reactivity in lupus may be partly hard-wired into the primary B-cell repertoire.Molecular immunology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Anti-nuclear antibodies constitute the hallmark of lupus. The NZM2410-derived Sle1 lupus susceptibility interval on murine chromosome 1 breaches tolerance, leading to the emergence of anti-nuclear autoantibodies targeting nucleosomes. However, little is known about the molecular structure of the anti-nucleosome autoantibodies from this genetically simplified mouse model of lupus. In this study, the immunoglobulin heavy chain and light chain sequences of 50 anti-nuclear monoclonal antibodies derived from five B6.Sle1(z) mice were compared to non-nuclear antibody controls. Compared to two different sets of non-nuclear antibodies, anti-nucleosome antibodies derived from B6.Sle1(z) congenic mice exhibited a high degree of clonal expansion and three distinct sequence motifs in their heavy chains - cationic CDR3 stretches, non-anionic CDR2 regions, and an increased frequency of aspartate residues at H50, which together increased the likelihood of an antibody being chromatin-reactive by approximately 4-fold.
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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.