ArticleAutoimmunity2014
Parasites alter the pathological phenotype of lupus nephritis.
Article in Autoimmunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Monocyte chemoattractant protein-1 (MCP-1)-2518 A/G polymorphism and lupus nephritis risk: A PRISMA-compliant meta-analysis.Medicine · 2017Pooled it
- Distinction Between Proliferative Lupus Nephritis and Membranous Lupus Nephritis Based on Inflammation, NETosis, and Glomerular Exostosin.International journal of molecular sciences · 2025Review
- Lupus-like membranous nephropathy during the postpartum period expressing glomerular antigens exostosin 1/exostosin 2 and phospholipase A2 receptor: a case report.CEN case reports · 2024Article
- Immunopathological analysis of the expression of glomerular exostosin 1 and exostosin 2 in Japanese patients with lupus nephritis.Virchows Archiv : an international journal of pathology · 2021Article
- Repeated administration of alpha-galactosylceramide ameliorates experimental lupus nephritis in mice.Scientific reports · 2018Article
- Parasite-Derived Proteins for the Treatment of Allergies and Autoimmune Diseases.Frontiers in microbiology · 2017Review
- Autoimmunity in 2014.Clinical reviews in allergy & immunology · 2015Review
- Unraveling the Hygiene Hypothesis of helminthes and autoimmunity: origins, pathophysiology, and clinical applications.BMC medicine · 2015Review
- The parasitic worm product ES-62 targets myeloid differentiation factor 88-dependent effector mechanisms to suppress antinuclear antibody production and proteinuria in MRL/lpr mice.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis is one of the most serious complications of systemic lupus erythematosus and manifests with considerable phenotypic and histological heterogeneity. In particular, diffuse proliferative lupus nephritis (DPLN) and membranous lupus nephritis (MLN) represent morphologic forms that are polar opposites. DPLN is associated with autoimmune responses dominated by Th1 immune response associated with high levels of interferon (IFN)-γ. In contrast, a Th2 cytokine response is associated with the pathogenesis of MLN. MRL/lpr mice develop human LN-like immune complex-associated nephritis and provide a suitable histological model for human DPLN. Infection with Schistosoma mansoni skewed a Th2-type immune response induction and IL-10 in MRL/lpr mice, drastically changing the pathophysiology of glomerulonephritis from DPLN to MLN accompanied by increased IgG1 and IgE in the sera. T cells in 32-week-old MRL/lpr mice infected with S. mansoni expressed significantly more IL-4 and IL-10 than T cells of uninfected mice; T cells with IFN-γ were comparable between infected and uninfected MR/lpr mice. Thus, the helminthic infection modified the cytokine microenvironment and altered the pathological phenotype of autoimmune nephritis.
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Registered trials
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