ArticleThe Journal of clinical investigation1999
Genetic dissection of lupus pathogenesis: a recipe for nephrophilic autoantibodies.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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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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Who cites it
61 citing papers in PubMed.
- Diffuse neuropsychiatric lupus: Clinical evidence, immune-mediated mechanisms, and therapeutic insights.Seminars in immunology · 2025Review
- KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes.Communications biology · 2024Article
- FasClinical immunology (Orlando, Fla.) · 2024Article
- Heterogeneity and clonality of kidney-infiltrating T cells in murine lupus nephritis.JCI insight · 2022Article
- Identification of polo-like kinase 1 as a therapeutic target in murine lupus.Clinical & translational immunology · 2022Article
- Cognitive Impairment in SLE: Mechanisms and Therapeutic Approaches.Current rheumatology reports · 2021Review
- Estrogen Receptor Alpha Signaling Is Responsible for the Female Sex Bias in the Loss of Tolerance and Immune Cell Activation Induced by the Lupus Susceptibility LocusFrontiers in immunology · 2020Article
- Lipocalin-2 is a pathogenic determinant and biomarker of neuropsychiatric lupus.Journal of autoimmunity · 2019Article
- DNA as a self-antigen: nature and regulation.Current opinion in immunology · 2018Review
- Mouse models of lupus: what they tell us and what they don't.Lupus science & medicine · 2018Article
- Monocyte Siglec-14 expression is upregulated in patients with systemic lupus erythematosus and correlates with lupus disease activity.Rheumatology (Oxford, England) · 2017Article
- PKK deficiency in B cells prevents lupus development in Sle lupus mice.Immunology letters · 2017Article
- Genetics and pathogenesis of systemic lupus erythematosus and lupus nephritis.Nature reviews. Nephrology · 2015Review
- Estrogen receptor alpha signaling promotes Sle1-induced loss of tolerance and immune cell activation and is responsible for sex bias in B6.Sle1 congenic mice.Clinical immunology (Orlando, Fla.) · 2015Article
- Class I and II histone deacetylase inhibition by ITF2357 reduces SLE pathogenesis in vivo.Clinical immunology (Orlando, Fla.) · 2014Article
- Identical twins:one with anti-glomerular basement membrane glomerulonephritis,the other with systemic lupus erythematosus.BMC nephrology · 2013Article
- Protein kinase Cβ is required for lupus development in Sle mice.Arthritis and rheumatism · 2013Article
- Lupus-prone strains vary in susceptibility to antibody-mediated end organ disease.Genes and immunity · 2013Article
- Article
- Ly9 (CD229) Cell-Surface Receptor is Crucial for the Development of Spontaneous Autoantibody Production to Nuclear Antigens.Frontiers in immunology · 2013Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Sle1 and Sle3 are 2 loci that confer susceptibility to lupus nephritis in the NZM2410 strain of mice. Our previous work has shown that B6.NZMc1 mice, congenic for Sle1, exhibit loss of tolerance to chromatin but do not develop any pathogenic autoantibodies or disease. B6.NZMc7 mice, congenic for Sle3, exhibit low-grade polyclonal B- and T-cell activation, elevated CD4/CD8 ratios, and mildly penetrant glomerulonephritis. In contrast to these monocongenics, the present study reveals that B6.NZMc1|c7 mice, bicongenic for Sle1 and Sle3, exhibit splenomegaly, significantly expanded populations of activated B and CD4(+) T cells, and a robust, variegated IgG autoantibody response targeting multiple components of chromatin (including double-stranded DNA), intact glomeruli, and basement membrane matrix antigens. As one might predict, these mice, particularly the females, exhibit highly penetrant glomerulonephritis. These findings lend strong support to a two-step epistatic model for the formation of pathogenic, nephrophilic autoantibodies in lupus. Whereas loci such as Sle1 may serve to breach tolerance to chromatin, full-blown pathogenic maturation of the autoantibody response appears to require additional input from other loci (such as Sle3) and gender-based factors.
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Registered trials
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