ArticleProceedings of the National Academy of Sciences of the United States of America1996
Amelioration of lupus-like autoimmune disease in NZB/WF1 mice after treatment with a blocking monoclonal antibody specific for complement component C5.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 339 citations in OpenAlex.
- Complement and kidney diseases: unlocking the opportunity of targeted treatments for glomerular diseases, including IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Review
- Cisplatin-induced acute kidney injury in lupus-prone NZB/W F1 mice: a potential experimental model of acute kidney injury superimposed on chronic kidney disease.The Journal of veterinary medical science · 2026Article
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- Damaged glomeruli in proliferative pediatric lupus nephritis exhibit a C5a-C5aR1 induced fibrotic transcriptional program.bioRxiv : the preprint server for biology · 2026Article
- Systemic lupus erythematosus as the paradigm for understanding the complex immune relationships and therapeutic opportunities for targeting complement in autoimmune diseases.Immunobiology · 2025Review
- Animal models of neuropsychiatric systemic lupus erythematosus: deciphering the complexity and guiding therapeutic development.Autoimmunity · 2024Review
- Enhanced medullary and extramedullary granulopoiesis sustain the inflammatory response in lupus nephritis.Lupus science & medicine · 2024Article
- Microvascular C5b-9 deposition in non-lesional skin in patients with SLE and its correlation with active lupus nephritis: a prospective observational study.Lupus science & medicine · 2023Observational
- Complement therapeutics are coming of age in rheumatology.Nature reviews. Rheumatology · 2023Review
- Relationship between neutrophil gelatinase-associated lipocalin levels and disease parameters including clinicopathological parameters and various cytokine levels in systemic lupus erythematosus.The Journal of veterinary medical science · 2023Article
- Microglia activation in the presence of intact blood-brain barrier and disruption of hippocampal neurogenesis via IL-6 and IL-18 mediate early diffuse neuropsychiatric lupus.Annals of the rheumatic diseases · 2023Article
- Promising Experimental Treatments for Lupus Nephritis: Key Talking Points and Potential Opportunities.Research and reports in urology · 2023Review
- Unraveling the Link between Interferon-α and Systemic Lupus Erythematosus: From the Molecular Mechanisms to Target Therapies.International journal of molecular sciences · 2022Review
- ATR-mediated DNA damage responses underlie aberrant B cell activity in systemic lupus erythematosus.Science advances · 2022Article
- Complement in Lupus: Biomarker, Therapeutic Target, or a Little Bit of Both?Kidney international reports · 2021Article
- Expanding the Role of Complement Therapies: The Case for Lupus Nephritis.Journal of clinical medicine · 2021Review
- Bite of the wolf: innate immune responses propagate autoimmunity in lupus.The Journal of clinical investigation · 2021Review
- Review
- Emerging Technologies to Study the Glomerular Filtration Barrier.Frontiers in medicine · 2021Review
- Punicalagin Ameliorates Lupus Nephritis via Inhibition of PAR2.International journal of molecular sciences · 2020Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
New Zealand black x New Zealand white (NZB/W) F1 mice spontaneously develop an autoimmune syndrome with notable similarities to human systemic lupus erythematosus. Female NZB/WF1 mice produce high titers of antinuclear antibodies and invariably succumb to severe glomerulonephritis by 12 months of age. Although the development of the immune-complex nephritis is accompanied by abundant local and systemic complement activation, the role of proinflammatory complement components in disease progression has not been established. In this study we have examined the contribution of activated terminal complement proteins to the pathogenesis of the lupus-like autoimmune disease. Female NZB/W F1 mice were treated with a monoclonal antibody (mAb) specific for the C5 component of complement that blocks the cleavage of C5 and thus prevents the generation of the potent proinflammatory factors C5a and C5b-9. Continuous therapy with anti-C5 mAb for 6 months resulted in significant amelioration of the course of glomerulonephritis and in markedly increased survival. These findings demonstrate an important role for the terminal complement cascade in the progression of renal disease in NZB/W F1 mice, and suggest that mAb-mediated C5 inhibition may be a useful approach to the therapy of immune-complex glomerulonephritis in humans.
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