ArticleThe Journal of clinical investigation2009
Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 108 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
108 citing papers in PubMed, 202 citations in OpenAlex.
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- Exploring the Relationship Between Immune Cells and Chronic Kidney Disease by Mendelian Randomization, Colocalization Analysis, and SMR.Mediators of inflammation · 2025Article
- Article
- Tissue-resident memory T cells break tolerance to renal autoantigens and orchestrate immune-mediated nephritis.Cellular & molecular immunology · 2024Article
- Abatacept Decreases Renal T-cell Infiltration and Renal Inflammation and Ameliorates Progressive Renal Injury in Obese Dahl Salt-sensitive Rats Before Puberty.Journal of cardiovascular pharmacology · 2024Article
- Underlying Mechanisms and Treatment of Hypertension in Glomerular Diseases.Current hypertension reports · 2024Review
- Integrated temporal transcriptional and epigenetic single-cell analysis reveals the intrarenal immune characteristics in an early-stage model of IgA nephropathy during its acute injury.Frontiers in immunology · 2024Article
- Rare Variants in Genes Encoding Subunits of the Epithelial NaHypertension (Dallas, Tex. : 1979) · 2022Article
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- Glomerulonephritis and autoimmune vasculitis are independent of P2RX7 but may depend on alternative inflammasome pathways.The Journal of pathology · 2022Article
- Digital Spatial Profiling of Individual Glomeruli From Patients With Anti-Neutrophil Cytoplasmic Autoantibody-Associated Glomerulonephritis.Frontiers in immunology · 2022Article
- New Onset Biopsy-Proven Nephropathies after COVID Vaccination.American journal of nephrology · 2022Article
- Delayed Onset Minimal Change Disease as a Manifestation of Lupus Podocytopathy.Clinics and practice · 2021Article
- Role of Dendritic Cell in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- Two faces of lupus nephritis? Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
- CCL17-producing cDC2s are essential in end-stage lupus nephritis and averted by a parasitic infection.The Journal of clinical investigation · 2021Article
- A Novel Inflammatory Dendritic Cell That Is Abundant and Contiguous to T Cells in the Kidneys of Patients With Lupus Nephritis.Frontiers in immunology · 2021Article
- New Aspects of Kidney Fibrosis-From Mechanisms of Injury to Modulation of Disease.Frontiers in medicine · 2021Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progression of kidney disease to renal failure correlates with infiltration of mononuclear immune cells into the tubulointerstitium. These infiltrates contain macrophages, DCs, and T cells, but the role of each cell type in disease progression is unclear. To investigate the underlying immune mechanisms, we generated transgenic mice that selectively expressed the model antigens ovalbumin and hen egg lysozyme in glomerular podocytes (NOH mice). Coinjection of ovalbumin-specific transgenic CD8+ CTLs and CD4+ Th cells into NOH mice resulted in periglomerular mononuclear infiltrates and inflammation of parietal epithelial cells, similar to lesions frequently observed in human chronic glomerulonephritis. Repetitive T cell injections aggravated infiltration and caused progression to structural and functional kidney damage after 4 weeks. Mechanistic analysis revealed that DCs in renal lymph nodes constitutively cross-presented ovalbumin and activated CTLs. These CTLs released further ovalbumin for CTL activation in the lymph nodes and for simultaneous presentation to Th cells by distinct DC subsets residing in the kidney tubulointerstitium. Crosstalk between tubulointerstitial DCs and Th cells resulted in intrarenal cytokine and chemokine production and in recruitment of more CTLs, monocyte-derived DCs, and macrophages. The importance of DCs was established by the fact that DC depletion rapidly resolved established kidney immunopathology. These findings demonstrate that glomerular antigen-specific CTLs and Th cells can jointly induce renal immunopathology and identify kidney DCs as a mechanistic link between glomerular injury and the progression of kidney disease.
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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.