ArticleJournal of the American Society of Nephrology : JASN2009
The IL-23/Th17 axis contributes to renal injury in experimental 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 118 papers.
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118 citing papers in PubMed, 243 citations in OpenAlex.
- Erythroid Atypical Chemokine Receptor 1 Deficiency Aggravates Immune-Mediated Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Integrated transcriptomic analysis of LMB2-induced podocyte injury identifies conserved inflammatory and adaptive stress responses.PloS one · 2026Article
- T-cell immunity in the experimental autoimmune vasculitis rat model.Journal of translational autoimmunity · 2025Article
- Divergent stage-specific regulation of neutrophil function by glucose transporter 1 in murine antibody-mediated glomerulonephritis.JCI insight · 2025Article
- Review
- Cyclosporine and fedratinib combination therapy via modulating Th17/Treg balance in Rat model of membranous glomerulonephritis.Biochemistry and biophysics reports · 2024Article
- Animal models of lupus nephritis: the past, present and a future outlook.Autoimmunity · 2024Review
- γδ T cells in immune-mediated kidney disease.European journal of immunology · 2024Review
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- Immune profiling-based targeting of pathogenic T cells with ustekinumab in ANCA-associated glomerulonephritis.Nature communications · 2024Article
- C/EBPδ Mediates Immunity to Renal Autoinflammatory Disorders in a Stage-specific Manner.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The RNA binding protein Arid5a drives IL-17-dependent autoantibody-induced glomerulonephritis.The Journal of experimental medicine · 2024Article
- The effect ofTranslational andrology and urology · 2024Article
- Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury.International journal of biological sciences · 2024Article
- Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease.Nature communications · 2023Article
- Chronic treatment with IL-25 increases renal M2 macrophages and reduces renal injury in obese Dahl salt-sensitive rats during the prepubescent stage.American journal of physiology. Renal physiology · 2023Article
- Review
- Association of genetic polymorphisms in IL-23R and IL-17A with the susceptibility to IgA nephropathy in a Chinese Han population.Genes and immunity · 2022Article
- Immunomodulatory Activity of Mesenchymal Stem Cells in Lupus Nephritis: Advances and Applications.Frontiers in immunology · 2022Review
- Interleukin-22 in Renal Protection and Its Pathological Role in Kidney Diseases.Frontiers in immunology · 2022Review
58 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cells infiltrate the kidney in both human and experimental glomerulonephritis, and several lines of evidence indicate that T cell-mediated tissue damage plays an important role in the immunopathogenesis of renal inflammatory diseases. However, the functions of the different T cell subsets, particularly the recently identified interleukin-17 (IL-17)-producing T cells (Th17 cells), are incompletely understood in glomerulonephritis. Here, we identified renal IL-17-producing T cells in the T cell-mediated model of nephrotoxic nephritis in mice. In vitro, IL-17 enhanced the production of the proinflammatory chemokines CCL2/MCP-1, CCL3/MIP-1alpha, and CCL20/LARC, which are implicated in the recruitment of T cells and monocytes, in mouse mesangial cells. To determine the function of Th17 cells in renal inflammation, we induced nephrotoxic nephritis in IL-23 p19(-/-) mice, which have reduced numbers of Th17 cells, and in IL-17(-/-) mice, which are deficient in the effector cytokine IL-17 itself. In comparison with nephritic wild-type mice, IL-23 p19(-/-) mice demonstrated less infiltration of Th17 cells, and both IL-23 p19(-/-) and IL-17(-/-) mice developed less severe nephritis as measured by renal function, albuminuria, and frequency of glomerular crescent formation. These results demonstrate that the IL-23/IL-17 pathway significantly contributes to renal tissue injury in experimental glomerulonephritis. Targeting the IL-23/Th17 axis may be a promising therapeutic strategy for the treatment of proliferative and crescentic glomerulonephritis.
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