ArticleThe Journal of experimental medicine2004
Breaking tolerance to double stranded DNA, nucleosome, and other nuclear antigens is not required for the pathogenesis of lupus glomerulonephritis.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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.
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Who cites it
58 citing papers in PubMed, 159 citations in OpenAlex.
- B1-cell-produced anti-phosphatidylserine antibodies contribute to lupus nephritis development via TLR-mediated Syk activation.Cellular & molecular immunology · 2023Article
- Molecular mechanisms governing the progression of nephritis in lupus prone mice and human lupus patients.Frontiers in immunology · 2023Article
- 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
- Interactions among glomerulus infiltrating macrophages and intrinsic cells via cytokines in chronic lupus glomerulonephritis.Journal of autoimmunity · 2020Article
- Nature of T cell epitopes in lupus antigens and HLA-DR determines autoantibody initiation and diversification.Annals of the rheumatic diseases · 2019Article
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- Protective Role of Hepcidin in Polymicrobial Sepsis and Acute Kidney Injury.Frontiers in pharmacology · 2019Article
- Pathogenesis of proliferative lupus nephritis from a historical and personal perspective.Clinical immunology (Orlando, Fla.) · 2017Review
- Podocyte Activation of NLRP3 Inflammasomes Contributes to the Development of Proteinuria in Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- Molecular and Immunological Basis of Tubulo-Interstitial Injury in Lupus Nephritis: a Comprehensive Review.Clinical reviews in allergy & immunology · 2017Review
- Modelling clinical systemic lupus erythematosus: similarities, differences and success stories.Rheumatology (Oxford, England) · 2017Review
- Recent advances in the understanding of renal inflammation and fibrosis in lupus nephritis.F1000Research · 2017Review
- Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis.Inflammation · 2016Article
- Role of Natural Autoantibodies and Natural IgM Anti-Leucocyte Autoantibodies in Health and Disease.Frontiers in immunology · 2016Review
- DNA-histone complexes as ligands amplify cell penetration and nuclear targeting of anti-DNA antibodies via energy-independent mechanisms.Immunology · 2016Article
- Changing the concepts of immune-mediated glomerular diseases through proteomics.Proteomics. Clinical applications · 2015Review
- Epidermal injury promotes nephritis flare in lupus-prone mice.Journal of autoimmunity · 2015Article
- A Central Role for HLA-DR3 in Anti-Smith Antibody Responses and Glomerulonephritis in a Transgenic Mouse Model of Spontaneous Lupus.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- The Role of Anti-DNA Antibodies in the Development of Lupus Nephritis: A Complementary, or Alternative, Viewpoint?Seminars in nephrology · 2015Review
- Anti-dsDNA Antibodies are one of the many autoantibodies in systemic lupus erythematosus.F1000Research · 2015Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
In lupus-prone NZM2328 mice, a locus Cgnz1 on chromosome 1 was linked to chronic glomerulonephritis, severe proteinuria, and early mortality in females. A locus Adnz1 on chromosome 4 was linked to antinuclear antibody (ANA) and anti-double stranded DNA (dsDNA) antibody (Ab) production. In this investigation, two congenic strains, NZM2328.C57L/Jc1 (NZM.C57Lc1) and NZM2328.C57L/Jc4 (NZM.C57Lc4), were generated by replacing the respective genetic intervals containing either Cgnz1 or Adnz1 with those from C57L/J, a nonlupus-prone strain. The NZM.C57Lc1 females had markedly reduced incidence of chronic glomerulonephritis and severe proteinuria. NZM.C57Lc4 females had chronic glomerulonephritis and severe proteinuria without circulating ANA, anti-dsDNA, and antinucleosome Ab. These data confirm the linkage analysis. Unexpectedly, NZM.C57Lc1 females had little anti-dsDNA and related Ab, suggesting the presence of a second locus Adnz2 on chromosome 1. The diseased NZM.C57Lc4 kidneys had immune complexes by immunofluorescence and electron microscopy. The eluates from these kidneys did not contain ANA, anti-dsDNA, and antinucleosome Ab, indicative of the presence of non-anti-dsDNA nephritogenic Ab. Thus, breaking tolerance to dsDNA and chromatin is not required for the pathogenesis of lupus nephritis. These results reaffirm that anti-dsDNA and related Ab production and chronic glomerulonephritis are under independent genetic control. These findings have significant implications in the pathogenesis of systemic lupus erythematosus.
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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.