ArticleProceedings of the National Academy of Sciences of the United States of America2001
The major murine systemic lupus erythematosus susceptibility locus, Sle1, is a cluster of functionally related genes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 321 citations in OpenAlex.
- Pbx1 as a regulator of T-cell fate in autoimmunity.Frontiers in immunology · 2026Review
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- NADPH oxidase exerts a B cell-intrinsic contribution to lupus risk by modulating endosomal TLR signals.The Journal of experimental medicine · 2024Article
- Lupus susceptibility geneScience advances · 2024Article
- SAP-expressing T peripheral helper cells identify systemic lupus erythematosus patients with lupus nephritis.Frontiers in immunology · 2024Article
- Spatial enrichment of the type 1 interferon signature in the brain of a neuropsychiatric lupus murine model.Brain, behavior, and immunity · 2023Article
- Characterization of Ly108-H1 Signaling Reveals Ly108-3 Expression and Additional Strain-Specific Differences in Lupus Prone Mice.International journal of molecular sciences · 2023Article
- Lupus Susceptibility Loci Predispose Mice to Clonal Lymphocytic Responses and Myeloid Expansion.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Polygenic autoimmune disease risk alleles impacting B cell tolerance act in concert across shared molecular networks in mouse and in humans.Frontiers in immunology · 2022Review
- Genetic Variations Controlling Regulatory T Cell Development and Activity in Mouse Models of Lupus-Like Autoimmunity.Frontiers in immunology · 2022Review
- Lupus susceptibility gene Esrrg modulates regulatory T cells through mitochondrial metabolism.JCI insight · 2021Article
- Context-Dependent miR-21 Regulation of TLR7-Mediated Autoimmune and Foreign Antigen-Driven Antibody-Forming Cell and Germinal Center Responses.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Review
- Autoimmune experimental orchitis and chronic glomerulonephritis with end stage renal disease are controlled by Cgnz1 for susceptibility to end organ damage.Clinical immunology (Orlando, Fla.) · 2021Article
- Genetic dissection of a major haplotype associated with arthritis reveal FcγR2b and FcγR3 to act additively.European journal of immunology · 2021Article
- miRNA-Mediated Control of B Cell Responses in Immunity and SLE.Frontiers in immunology · 2021Review
- Inhibition of B cell activation followingJournal of translational autoimmunity · 2021Article
- SLAM Associated Protein Signaling in T Cells: Tilting the Balance Toward Autoimmunity.Frontiers in immunology · 2021Review
- T cells expressing the lupus susceptibility allele Pbx1d enhance autoimmunity and atherosclerosis in dyslipidemic mice.JCI insight · 2020Article
- T cell metabolism: new insights in systemic lupus erythematosus pathogenesis and therapy.Nature reviews. Rheumatology · 2020Review
72 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The major murine systemic lupus erythematosus (SLE) susceptibility locus Sle1 is syntenic to a chromosomal region linked with SLE susceptibility in multiple human studies. Congenic analyses have shown that Sle1 breaks tolerance to chromatin, a necessary step for full disease induction that can be suppressed by specific modifier loci. In the present study, our fine mapping analysis of the location of Sle1 has determined that three loci within this congenic interval, termed Sle1a, Sle1b, and Sle1c, can independently cause a loss of tolerance to chromatin. Each displays a distinctive profile of serological and cellular characteristics, with T and B cell functions being more affected by Sle1a and Sle1b, respectively. The epistatic interactions of Sle1 with other susceptibility loci to cause severe nephritis cannot be accounted, however, by these three loci alone, suggesting the existence of an additional locus, termed Sle1d. These findings indicate that the potent autoimmune phenotype caused by the Sle1 genomic interval reflects the combined impact of four, separate, susceptibility genes. This level of genetic complexity, combined with similar findings in other systems, supports the possibility that many complex trait loci reflect the impact of polymorphisms in linked clusters of genes with related functions.
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