ArticleJournal of the American Society of Nephrology : JASN2016
CD103+ Dendritic Cells Elicit CD8+ T Cell Responses to Accelerate Kidney Injury in Adriamycin Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 57 citations in OpenAlex.
- Animal models of anemia of inflammation: Methodological advances, limitations, and translational applications.Animal models and experimental medicine · 2026Review
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- IKZF1 as a potential therapeutic target for dendritic cell-mediated immunotherapy in IgA nephropathy.Cell communication and signaling : CCS · 2025Article
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- Exploring the Relationship Between Immune Cells and Chronic Kidney Disease by Mendelian Randomization, Colocalization Analysis, and SMR.Mediators of inflammation · 2025Article
- Adenine-induced animal model of chronic kidney disease: current applications and future perspectives.Renal failure · 2024Review
- Acquired immunostimulatory phenotype of migratory CD103+ DCs promotes alloimmunity following corneal transplantation.JCI insight · 2024Article
- Entinostat, nivolumab and ipilimumab for women with advanced HER2-negative breast cancer: a phase Ib trial.Nature cancer · 2024Article
- Recent Advances in Understanding Peripheral and Gut Immune Cell-Mediated Salt-Sensitive Hypertension and Nephropathy.Hypertension (Dallas, Tex. : 1979) · 2024Review
- CD8 T cells induce the peritubular capillary rarefaction during AKI to CKD transition.International journal of biological sciences · 2024Article
- Mechanistic insights into the interaction between the host gut microbiome and malaria.PLoS pathogens · 2023Review
- Immune responses in the uterine mucosa: clues for vaccine development in pigs.Frontiers in immunology · 2023Review
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- IL-23 signaling prevents ferroptosis-driven renal immunopathology during candidiasis.Nature communications · 2022Article
- M2c Macrophages Protect Mice from Adriamycin-Induced Nephropathy by Upregulating CD62L in Tregs.Mediators of inflammation · 2022Article
- Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration.JCI insight · 2021Article
- Role of Dendritic Cell in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- A flow cytometry approach reveals heterogeneity in conventional subsets of murine renal mononuclear phagocytes.Scientific reports · 2021Article
- Lung CD103American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Conventional Type 1 Dendritic Cells (cDC1) in Human Kidney Diseases: Clinico-Pathological Correlations.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD103(+) dendritic cells (DCs) in nonlymphoid organs exhibit two main functions: maintaining tolerance by induction of regulatory T cells and protecting against tissue infection through cross-presentation of foreign antigens to CD8(+) T cells. However, the role of CD103(+) DCs in kidney disease is unknown. In this study, we show that CD103(+) DCs are one of four subpopulations of renal mononuclear phagocytes in normal kidneys. CD103(+) DCs expressed DC-specific surface markers, transcription factors, and growth factor receptors and were found in the kidney cortex but not in the medulla. The number of kidney CD103(+) DCs was significantly higher in mice with adriamycin nephropathy (AN) than in normal mice, and depletion of CD103(+) DCs attenuated kidney injury in AN mice. In vitro, kidney CD103(+) DCs preferentially primed CD8(+) T cells and did not directly induce tubular epithelial cell apoptosis. Adoptive transfer of CD8(+) T cells significantly exacerbated kidney injury in AN SCID mice, whereas depletion of CD103(+) DCs in these mice impaired activation and proliferation of transfused CD8(+) T cells and prevented the exacerbation of kidney injury associated with this transfusion. In conclusion, kidney CD103(+) DCs display a pathogenic role in murine CKD via activation of CD8(+) T cells.
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