ArticleJournal of the American Society of Nephrology : JASN2009
Th1 and Th17 cells induce proliferative glomerulonephritis.
Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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.
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
83 citing papers in PubMed, 162 citations in OpenAlex.
- Article
- Prospective Pilot Study of Lavender Terpenoid Topical Formulation in Psoriasis Patients with Chronic Kidney Disease: Clinical and Inflammatory Outcomes.Biomedicines · 2026Article
- The role of gut microbiota dysbiosis in the pathogenesis of hyperuricemic nephropathy.Frontiers in molecular biosciences · 2026Review
- T-cell immunity in the experimental autoimmune vasculitis rat model.Journal of translational autoimmunity · 2025Article
- Immune imbalance mediates the relationship between plasma vitamin D concentration and preeclampsia in Chinese pregnant women: a case-control study.Frontiers in nutrition · 2025Article
- Immune cell signatures and inflammatory mediators: unraveling their genetic impact on chronic kidney disease through Mendelian randomization.Clinical and experimental medicine · 2024Article
- Association between Psoriasis and Renal Functions: An Integration Study of Observational Study and Mendelian Randomization.Biomedicines · 2024Article
- Macrophage-derived macrophage migration inhibitory factor mediates renal injury in anti-glomerular basement membrane glomerulonephritis.Frontiers in immunology · 2024Article
- Glomerulonephritis: immunopathogenesis and immunotherapy.Nature reviews. Immunology · 2023Review
- Review
- The Th17 Pathway in Vascular Inflammation: Culprit or Consort?Frontiers in immunology · 2022Review
- Immune cell behaviour and dynamics in the kidney - insights from in vivo imaging.Nature reviews. Nephrology · 2022Review
- Regulatory role and mechanisms of myeloid TLR4 in anti-GBM glomerulonephritis.Cellular and molecular life sciences : CMLS · 2021Article
- T cell plasticity in renal autoimmune disease.Cell and tissue research · 2021Review
- The role of Treg subtypes in glomerulonephritis.Cell and tissue research · 2021Review
- Ixekizumab May Improve Renal Function in Psoriasis.Healthcare (Basel, Switzerland) · 2021Article
- Crescentic Glomerulonephritis: Pathogenesis and Therapeutic Potential of Human Amniotic Stem Cells.Frontiers in physiology · 2021Review
- Review
- Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice.International journal of molecular sciences · 2020Article
- Co-inhibitory Receptor Signaling in T-Cell-Mediated Autoimmune Glomerulonephritis.Frontiers in medicine · 2020Review
23 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
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.
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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.