ArticleImmunology2004
Autoimmunity and glomerulonephritis in mice with targeted deletion of the serum amyloid P component gene: SAP deficiency or strain combination?
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 62 citations in OpenAlex.
- Randomized phase I trial HIV-CORE 003: Depletion of serum amyloid P component and immunogenicity of DNA vaccination against HIV-1.PloS one · 2018Trial
- Cell-Free DNA (cfDNA), Its Applications in Cancer Diagnosis and Monitoring, and Its Potential Role in Regulating Cancer Metabolism.Advances in experimental medicine and biology · 2026Review
- Cell-Free DNA in the Pathogenesis and Therapy of Non-Infectious Inflammations and Tumors.Biomedicines · 2022Review
- 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
- Serum amyloid P deposition is a sensitive and specific feature of membranous-like glomerulopathy with masked IgG kappa deposits.Kidney international · 2020Article
- Anti-Pentraxin Antibodies in Autoimmune Diseases: Bystanders or Pathophysiological Actors?Frontiers in immunology · 2020Review
- Cell-Free DNA as a Biomarker in Autoimmune Rheumatic Diseases.Frontiers in immunology · 2019Review
- Neuroinflammation in Alzheimer's disease: Pleiotropic roles for cytokines and neuronal pentraxins.Behavioural brain research · 2018Review
- The Pentraxins 1975-2018: Serendipity, Diagnostics and Drugs.Frontiers in immunology · 2018Review
- Cell death in the pathogenesis of systemic lupus erythematosus and lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- European Veterinary Renal Pathology Service: A Survey Over a 7-Year Period (2008-2015).Journal of veterinary internal medicine · 2017Article
- Clearance Deficiency and Cell Death Pathways: A Model for the Pathogenesis of SLE.Frontiers in immunology · 2016Review
- Inhibition of murine fibrocyte differentiation by cross-linked IgG is dependent on FcγRI.Journal of leukocyte biology · 2014Article
- Pentraxins: structure, function, and role in inflammation.ISRN inflammation · 2013Review
- New features of invasive candidiasis in humans: amyloid formation by fungi and deposition of serum amyloid P component by the host.The Journal of infectious diseases · 2012Article
- Isolation and characterization of pharmaceutical grade human pentraxins, serum amyloid P component and C-reactive protein, for clinical use.Journal of immunological methods · 2012Article
- Serum amyloid P component facilitates DNA clearance and inhibits plasmid transfection: implications for human DNA vaccine.Gene therapy · 2012Article
- NETs: the missing link between cell death and systemic autoimmune diseases?Frontiers in immunology · 2012Article
- Article
- The role of defective clearance of apoptotic cells in systemic autoimmunity.Nature reviews. Rheumatology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Human serum amyloid P component (SAP) binds avidly to DNA, chromatin and apoptotic cells in vitro and in vivo. 129/Sv x C57BL/6 mice with targeted deletion of the SAP gene spontaneously develop antinuclear autoantibodies and immune complex glomerulonephritis. SAP-deficient animals, created by backcrossing the 129/Sv SAP gene deletion into pure line C57BL/6 mice and studied here for the first time, also spontaneously developed broad spectrum antinuclear autoimmunity and proliferative immune complex glomerulonephritis but without proteinuria, renal failure, or increased morbidity or mortality. Mice hemizygous for the SAP gene deletion had an intermediate autoimmune phenotype. Injected apoptotic cells and isolated chromatin were more immunogenic in SAP(-/-) mice than in wild-type mice. In contrast, SAP-deficient pure line 129/Sv mice did not produce significant autoantibodies either spontaneously or when immunized with extrinsic chromatin or apoptotic cells, indicating that loss of tolerance is markedly strain dependent. However, SAP deficiency in C57BL/6 mice only marginally affected plasma clearance of exogenous chromatin and had no effect on distribution of exogenous nucleosomes between the liver and kidneys, which were the only tissue sites of catabolism. Furthermore, transgenic expression of human SAP in the C57BL/6 SAP knockout mice did not abrogate the autoimmune phenotype. This may reflect the different binding affinities of mouse and human SAP for nuclear autoantigens and/or the heterologous nature of transgenic human SAP in the mouse. Alternatively, the autoimmunity may be independent of SAP deficiency and caused by expression of 129/Sv chromosome 1 genes in the C57BL/6 background.
Indexed as
Identifiers
What OpenQuestion holds
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.