ArticleThe Journal of experimental medicine2006
Pathology and protection in nephrotoxic nephritis is determined by selective engagement of specific Fc receptors.
Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 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
107 citing papers in PubMed, 243 citations in OpenAlex.
- Sialylation of IgG Fc domain impairs complement-dependent cytotoxicity.The Journal of clinical investigation · 2015Trial
- The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- More Than Just Antinuclear Antibodies: IgG Sialylation May Tip the Balance in Autoimmunity.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- Soluble Factors and Mechanisms Regulated by Sialylated IgG Signaling.Immunological reviews · 2025Review
- Immunoglobulins: Mechanistic Approaches in Moderation of Various Inflammatory and Anti-inflammatory Pathways.Current pharmaceutical biotechnology · 2025Review
- Role of Antibody Glycosylation in Health, Disease, and Therapy.Handbook of experimental pharmacology · 2025Review
- Animal models of lupus nephritis: the past, present and a future outlook.Autoimmunity · 2024Review
- Gasdermin D deficiency aborts myeloid calcium influx to drive granulopoiesis in lupus nephritis.Cell communication and signaling : CCS · 2024Article
- Transcriptome Analysis of BAFF/BAFF-R System in Murine Nephrotoxic Serum Nephritis.International journal of molecular sciences · 2024Article
- An engineered immunomodulatory IgG1 Fc suppresses autoimmune inflammation through pathways shared with i.v. immunoglobulin.The Journal of clinical investigation · 2024Article
- Group 3 Innate Lymphoid Cells Exacerbate Lupus Nephritis by Promoting B Cell Activation in Kidney Ectopic Lymphoid Structures.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Review
- Kidney tubular epithelial cell ferroptosis links glomerular injury to tubulointerstitial pathology in lupus nephritis.Clinical immunology (Orlando, Fla.) · 2023Article
- Therapeutic effects of Fc gamma RIV inhibition are mediated by selectively blocking immune complex-induced neutrophil activation in epidermolysis bullosa acquisita.Frontiers in immunology · 2022Article
- Review
- Deletions inCell reports. Medicine · 2021Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction of heterologous anti-glomerular basement membrane antiserum (nephrotoxic serum, NTS) into presensitized mice triggers the production of IgG anti-NTS antibodies that are predominantly IgG2b and the glomerular deposition of pathogenic immune complexes, leading to accelerated renal disease. The pathology observed in this model is determined by the effector cell activation threshold that is established by the coexpression on infiltrating macrophages of the IgG2a/2b restricted activation receptor FcgammaRIV and its inhibitory receptor counterpart, FcgammaRIIB. Blocking FcgammaRIV with a specific monoclonal antibody thereby preventing IgG2b engagement or treatment with high dose intravenous gamma-globulin (IVIG) to down-regulate FcgammaRIV while up-regulating FcgammaRIIB, protects mice from fatal disease. In the absence of FcgammaRIIB, IVIG is not protective; this indicates that reduced FcgammaRIV expression alone is insufficient to protect animals from pathogenic IgG2b immune complexes. These results establish the significance of specific IgG subclasses and their cognate FcgammaRs in renal disease.
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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.